Category:Antihypertensives - Revision history

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	The transformative class of the antihypertensive era was the angiotensin-converting enzyme inhibitor. In 1965 the Brazilian physiologist [[wikipedia:Sérgio Henrique Ferreira\|Sérgio Ferreira]], working in [[wikipedia:John Vane\|John Vane]]'s laboratory in London, had isolated from the venom of the Brazilian pit viper Bothrops jararaca a series of small peptides that potentiated the action of bradykinin and inhibited the enzyme that converts angiotensin I to angiotensin II; the profound hypotension of a jararaca envenomation is in part the work of these peptides.<ref name="ferreira1965">Ferreira SH. A bradykinin-potentiating factor (BPF) present in the venom of ''Bothrops jararaca''. ''British Journal of Pharmacology and Chemotherapy''. 1965 Feb;24:163-169. PMID 14302350.</ref> A decade later [[wikipedia:Miguel Ondetti\|Miguel Ondetti]] and [[wikipedia:David Cushman (scientist)\|David Cushman]] at the [[wikipedia:Squibb\|Squibb Institute for Medical Research]], working from a model of the active site informed by what was then known of carboxypeptidase A, designed [[Captopril\|captopril]], a small orally bioavailable inhibitor of the converting enzyme.<ref name="ondetti1977">Ondetti MA, Rubin B, Cushman DW. Design of specific inhibitors of angiotensin-converting enzyme: new class of orally active antihypertensive agents. ''Science''. 1977 Apr 22;196(4288):441-444. PMID 191908.</ref> Captopril was approved by the U.S. Food and Drug Administration in 1981 and the class expanded quickly: [[Enalapril\|enalapril]], [[Lisinopril\|lisinopril]], [[Ramipril\|ramipril]], [[Benazepril\|benazepril]]. The [[:Category:Angiotensin_receptor_blockers\|angiotensin receptor blockers]] followed, beginning with [[Losartan\|losartan]] in 1995, developed at the DuPont Merck laboratories from a series of imidazole leads first reported by Takeda chemistry.<ref name="carini1991">Carini DJ, Duncia JV, Aldrich PE, Chiu AT, Johnson AL, Pierce ME, Price WA, Santella JB 3rd, Wells GJ, Wexler RR, et al. Nonpeptide angiotensin II receptor antagonists: the discovery of a series of N-(biphenylylmethyl)imidazoles as potent, orally active antihypertensives. ''Journal of Medicinal Chemistry''. 1991 Aug;34(8):2525-2547. PMID 1875347.</ref>		The transformative class of the antihypertensive era was the angiotensin-converting enzyme inhibitor. In 1965 the Brazilian physiologist [[wikipedia:Sérgio Henrique Ferreira\|Sérgio Ferreira]], working in [[wikipedia:John Vane\|John Vane]]'s laboratory in London, had isolated from the venom of the Brazilian pit viper Bothrops jararaca a series of small peptides that potentiated the action of bradykinin and inhibited the enzyme that converts angiotensin I to angiotensin II; the profound hypotension of a jararaca envenomation is in part the work of these peptides.<ref name="ferreira1965">Ferreira SH. A bradykinin-potentiating factor (BPF) present in the venom of ''Bothrops jararaca''. ''British Journal of Pharmacology and Chemotherapy''. 1965 Feb;24:163-169. PMID 14302350.</ref> A decade later [[wikipedia:Miguel Ondetti\|Miguel Ondetti]] and [[wikipedia:David Cushman (scientist)\|David Cushman]] at the [[wikipedia:Squibb\|Squibb Institute for Medical Research]], working from a model of the active site informed by what was then known of carboxypeptidase A, designed [[Captopril\|captopril]], a small orally bioavailable inhibitor of the converting enzyme.<ref name="ondetti1977">Ondetti MA, Rubin B, Cushman DW. Design of specific inhibitors of angiotensin-converting enzyme: new class of orally active antihypertensive agents. ''Science''. 1977 Apr 22;196(4288):441-444. PMID 191908.</ref> Captopril was approved by the U.S. Food and Drug Administration in 1981 and the class expanded quickly: [[Enalapril\|enalapril]], [[Lisinopril\|lisinopril]], [[Ramipril\|ramipril]], [[Benazepril\|benazepril]]. The [[:Category:Angiotensin_receptor_blockers\|angiotensin receptor blockers]] followed, beginning with [[Losartan\|losartan]] in 1995, developed at the DuPont Merck laboratories from a series of imidazole leads first reported by Takeda chemistry.<ref name="carini1991">Carini DJ, Duncia JV, Aldrich PE, Chiu AT, Johnson AL, Pierce ME, Price WA, Santella JB 3rd, Wells GJ, Wexler RR, et al. Nonpeptide angiotensin II receptor antagonists: the discovery of a series of N-(biphenylylmethyl)imidazoles as potent, orally active antihypertensives. ''Journal of Medicinal Chemistry''. 1991 Aug;34(8):2525-2547. PMID 1875347.</ref>

	The [[:Category:Calcium_channel_blockers\|calcium channel blockers]] entered cardiovascular medicine through a separate door. [[Verapamil\|Verapamil]], synthesized in Germany in 1962, was the first agent shown by [[wikipedia:Albrecht Fleckenstein\|Albrecht Fleckenstein]] to block the slow inward calcium current of cardiac and vascular smooth muscle.<ref name="fleckenstein1983">Fleckenstein A. History of calcium antagonists. ''Circulation Research''. 1983 Feb;52(2 Pt 2):I3-16. PMID 6297830.</ref> [[Nifedipine\|Nifedipine]] and the rest of the dihydropyridine family followed; [[Amlodipine\|amlodipine]], with its long plasma half-life and gradual onset, provided in 1992 the once-daily dosing and freedom from reflex tachycardia that the immediate-release dihydropyridines had lacked. By the end of the twentieth century five ~~medication~~ classes, the diuretics, the ACE inhibitors, the angiotensin receptor blockers, the calcium channel blockers, and the beta-blockers, were established as the building blocks of essential-hypertension therapy.		The [[:Category:Calcium_channel_blockers\|calcium channel blockers]] entered cardiovascular medicine through a separate door. [[Verapamil\|Verapamil]], synthesized in Germany in 1962, was the first agent shown by [[wikipedia:Albrecht Fleckenstein\|Albrecht Fleckenstein]] to block the slow inward calcium current of cardiac and vascular smooth muscle.<ref name="fleckenstein1983">Fleckenstein A. History of calcium antagonists. ''Circulation Research''. 1983 Feb;52(2 Pt 2):I3-16. PMID 6297830.</ref> [[Nifedipine\|Nifedipine]] and the rest of the dihydropyridine family followed; [[Amlodipine\|amlodipine]], with its long plasma half-life and gradual onset, provided in 1992 the once-daily dosing and freedom from reflex tachycardia that the immediate-release dihydropyridines had lacked. By the end of the twentieth century five medicine classes, the diuretics, the ACE inhibitors, the angiotensin receptor blockers, the calcium channel blockers, and the beta-blockers, were established as the building blocks of essential-hypertension therapy.

	The remaining clinical question, and it remains alive, is the treatment target. The early VA trials set a working aim of "below 140/90" by convention. The Hypertension Optimal Treatment trial in 1998 examined diastolic targets between 80 and 90 millimetres of mercury and could not show clear benefit of the lower one.<ref name="hot1998">Hansson L, Zanchetti A, Carruthers SG, Dahlöf B, Elmfeldt D, Julius S, Ménard J, Rahn KH, Wedel H, Westerling S, for the HOT Study Group. Effects of intensive blood-pressure lowering and low-dose aspirin in patients at high risk of cardiovascular disease: principal results of the Hypertension Optimal Treatment (HOT) randomised trial. ''Lancet''. 1998 Jun 13;351(9118):1755-1762. PMID 9635947.</ref> The Systolic Blood Pressure Intervention Trial in 2015, by contrast, randomized patients at high cardiovascular risk to a systolic target of 120 versus 140 and was stopped early for benefit in the intensive arm, at the cost of a higher rate of hypotension, syncope, and acute kidney injury.<ref name="sprint2015">SPRINT Research Group, Wright JT Jr, Williamson JD, Whelton PK, Snyder JK, Sink KM, Rocco MV, Reboussin DM, Rahman M, Oparil S, et al. A randomized trial of intensive versus standard blood-pressure control. ''New England Journal of Medicine''. 2015 Nov 26;373(22):2103-2116. PMID 26551272.</ref> Current American guidelines have settled, for most adults, on a treatment goal of less than 130/80 millimetres of mercury, while acknowledging that the evidence base for any single threshold remains contested and that the absolute benefit of treatment scales with the patient's baseline cardiovascular risk rather than with the blood pressure alone.<ref name="whelton2018">Whelton PK, Carey RM, Aronow WS, Casey DE Jr, Collins KJ, Dennison Himmelfarb C, DePalma SM, Gidding S, Jamerson KA, Jones DW, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults. ''Hypertension''. 2018 Jun;71(6):e13-e115. PMID 29133356.</ref>		The remaining clinical question, and it remains alive, is the treatment target. The early VA trials set a working aim of "below 140/90" by convention. The Hypertension Optimal Treatment trial in 1998 examined diastolic targets between 80 and 90 millimetres of mercury and could not show clear benefit of the lower one.<ref name="hot1998">Hansson L, Zanchetti A, Carruthers SG, Dahlöf B, Elmfeldt D, Julius S, Ménard J, Rahn KH, Wedel H, Westerling S, for the HOT Study Group. Effects of intensive blood-pressure lowering and low-dose aspirin in patients at high risk of cardiovascular disease: principal results of the Hypertension Optimal Treatment (HOT) randomised trial. ''Lancet''. 1998 Jun 13;351(9118):1755-1762. PMID 9635947.</ref> The Systolic Blood Pressure Intervention Trial in 2015, by contrast, randomized patients at high cardiovascular risk to a systolic target of 120 versus 140 and was stopped early for benefit in the intensive arm, at the cost of a higher rate of hypotension, syncope, and acute kidney injury.<ref name="sprint2015">SPRINT Research Group, Wright JT Jr, Williamson JD, Whelton PK, Snyder JK, Sink KM, Rocco MV, Reboussin DM, Rahman M, Oparil S, et al. A randomized trial of intensive versus standard blood-pressure control. ''New England Journal of Medicine''. 2015 Nov 26;373(22):2103-2116. PMID 26551272.</ref> Current American guidelines have settled, for most adults, on a treatment goal of less than 130/80 millimetres of mercury, while acknowledging that the evidence base for any single threshold remains contested and that the absolute benefit of treatment scales with the patient's baseline cardiovascular risk rather than with the blood pressure alone.<ref name="whelton2018">Whelton PK, Carey RM, Aronow WS, Casey DE Jr, Collins KJ, Dennison Himmelfarb C, DePalma SM, Gidding S, Jamerson KA, Jones DW, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults. ''Hypertension''. 2018 Jun;71(6):e13-e115. PMID 29133356.</ref>
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	== Classes indexed ==		== Classes indexed ==

	The principal ~~medication~~ classes by which the arterial blood pressure is lowered in modern practice:		The principal medicine classes by which the arterial blood pressure is lowered in modern practice:

	* [[:Category:ACE_inhibitors\|Angiotensin-converting enzyme (ACE) inhibitors]]: [[Benazepril\|benazepril]], [[Enalapril\|enalapril]], [[Lisinopril\|lisinopril]], [[Ramipril\|ramipril]]		* [[:Category:ACE_inhibitors\|Angiotensin-converting enzyme (ACE) inhibitors]]: [[Benazepril\|benazepril]], [[Enalapril\|enalapril]], [[Lisinopril\|lisinopril]], [[Ramipril\|ramipril]]

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An '''antihypertensive''' is a medicine that lowers the arterial blood pressure. The category, as a category of useful medicines, did not exist until the middle of the twentieth century, for the simple reason that high blood pressure was not, until then, understood to be a treatable disease. In 1931 the British physician [[wikipedia:John Hay (cardiologist)|John Hay]] set down the prevailing view in two sentences that became infamous: "There is some truth in the saying that the greatest danger to a man with a high blood pressure lies in its discovery, because then some fool is certain to try and reduce it."<ref name="hay1931">Hay J. The significance of a raised blood pressure. ''British Medical Journal''. 1931 Jul 11;2(3679):43-47.</ref> The reasoning behind the view was not unreasonable on its face: the elevated pressure was thought to be a compensatory response to a narrowed and hardened circulation, and the fear was that lowering it would reduce perfusion of the brain, the heart, and the kidneys to dangerous levels.

The view was dramatized publicly by the death of [[wikipedia:Franklin D. Roosevelt|President Franklin D. Roosevelt]] on the afternoon of 12 April 1945, of a massive cerebral hemorrhage at the age of sixty-three. His personal physician [[wikipedia:Howard Bruenn|Howard Bruenn]] later published the clinical record: pressures in the months before death of 240/130 millimetres of mercury, treated, in the absence of any effective option, with phenobarbital, digitalis, and bed rest, and rising to 300/190 at the time of the fatal stroke.<ref name="bruenn1970">Bruenn HG. Clinical notes on the illness and death of President Franklin D. Roosevelt. ''Annals of Internal Medicine''. 1970 Apr;72(4):579-591. PMID 4938425.</ref> The case has been reviewed many times in the decades since, both as a clinical history and as an argument that the medical profession had been wrong.

The argument was settled, formally, by [[wikipedia:Edward D. Freis|Edward Freis]] and the Veterans Administration Cooperative Study Group on Antihypertensive Agents, working at the Washington VA Hospital. Their first trial, published in 1967, randomized 143 men with diastolic pressures between 115 and 129 millimetres of mercury to either a combination of hydrochlorothiazide, reserpine, and hydralazine, or to placebo; the placebo arm accumulated strokes, heart failure, and aortic dissections at such a rate that the trial was stopped early and the protocol unblinded.<ref name="va1967">Veterans Administration Cooperative Study Group on Antihypertensive Agents. Effects of treatment on morbidity in hypertension. Results in patients with diastolic blood pressures averaging 115 through 129 mm Hg. ''JAMA''. 1967 Dec 11;202(11):1028-1034. PMID 4862632.</ref> A second VA Cooperative trial, in milder hypertension, confirmed the benefit in 1970.<ref name="va1970">Veterans Administration Cooperative Study Group on Antihypertensive Agents. Effects of treatment on morbidity in hypertension. II. Results in patients with diastolic blood pressure averaging 90 through 114 mm Hg. ''JAMA''. 1970 Aug 17;213(7):1143-1152. PMID 5468336.</ref> Observational data accumulating in parallel from the [[wikipedia:Framingham Heart Study|Framingham Heart Study]] showed that the relationship between blood pressure and cardiovascular events was continuous and monotonic, with no apparent threshold of harm.<ref name="kannel1996">Kannel WB. Blood pressure as a cardiovascular risk factor: prevention and treatment. ''JAMA''. 1996 May 22-29;275(20):1571-1576. PMID 8622248.</ref> The 1931 doctrine was abandoned and clinical attention shifted to which medicines to use, and at what blood-pressure target.

Several medicines were already in hand by 1967. The [[:Category:Thiazide_diuretics|thiazide diuretics]] had been introduced in 1957 with chlorothiazide, developed at the [[wikipedia:Merck Sharp & Dohme|Sharp and Dohme]] research laboratories by [[wikipedia:Karl H. Beyer|Karl Beyer]]'s group from an effort to improve on the existing carbonic anhydrase inhibitors; the new compound preferentially blocked sodium and chloride reabsorption in the distal tubule of the nephron and lowered the blood pressure as efficiently as it cleared the edema of heart failure.<ref name="beyer1993">Beyer KH Jr. Chlorothiazide. How the thiazides evolved as antihypertensive therapy. ''Hypertension''. 1993 Sep;22(3):388-391. PMID 8349333.</ref> [[Hydrochlorothiazide]], a closer derivative, followed two years later and became the standard of the class. The [[:Category:Direct_vasodilators|direct vasodilators]] had been developed earlier: [[Hydralazine|hydralazine]] at [[wikipedia:Ciba (company)|Ciba]] in 1949 as an offshoot of antimalarial chemistry, [[wikipedia:Minoxidil|minoxidil]] at [[wikipedia:Upjohn|Upjohn]] in the 1960s. The centrally acting sympatholytic [[wikipedia:Methyldopa|methyldopa]] was introduced by [[wikipedia:Merck & Co.|Merck]] in 1960. The [[:Category:Beta-blockers|beta-adrenergic blockers]], beginning with propranolol synthesized by [[wikipedia:James Black (pharmacologist)|James Black]] at [[wikipedia:Imperial Chemical Industries|Imperial Chemical Industries]] in 1964, lowered blood pressure as a side benefit of their antianginal effect, and were quickly recognized as antihypertensive in their own right.<ref name="black1964">Black JW, Crowther AF, Shanks RG, Smith LH, Dornhorst AC. A new adrenergic beta-receptor antagonist. ''Lancet''. 1964 May 16;1(7342):1080-1081. PMID 14132613.</ref>

The transformative class of the antihypertensive era was the angiotensin-converting enzyme inhibitor. In 1965 the Brazilian physiologist [[wikipedia:Sérgio Henrique Ferreira|Sérgio Ferreira]], working in [[wikipedia:John Vane|John Vane]]'s laboratory in London, had isolated from the venom of the Brazilian pit viper Bothrops jararaca a series of small peptides that potentiated the action of bradykinin and inhibited the enzyme that converts angiotensin I to angiotensin II; the profound hypotension of a jararaca envenomation is in part the work of these peptides.<ref name="ferreira1965">Ferreira SH. A bradykinin-potentiating factor (BPF) present in the venom of ''Bothrops jararaca''. ''British Journal of Pharmacology and Chemotherapy''. 1965 Feb;24:163-169. PMID 14302350.</ref> A decade later [[wikipedia:Miguel Ondetti|Miguel Ondetti]] and [[wikipedia:David Cushman (scientist)|David Cushman]] at the [[wikipedia:Squibb|Squibb Institute for Medical Research]], working from a model of the active site informed by what was then known of carboxypeptidase A, designed [[Captopril|captopril]], a small orally bioavailable inhibitor of the converting enzyme.<ref name="ondetti1977">Ondetti MA, Rubin B, Cushman DW. Design of specific inhibitors of angiotensin-converting enzyme: new class of orally active antihypertensive agents. ''Science''. 1977 Apr 22;196(4288):441-444. PMID 191908.</ref> Captopril was approved by the U.S. Food and Drug Administration in 1981 and the class expanded quickly: [[Enalapril|enalapril]], [[Lisinopril|lisinopril]], [[Ramipril|ramipril]], [[Benazepril|benazepril]]. The [[:Category:Angiotensin_receptor_blockers|angiotensin receptor blockers]] followed, beginning with [[Losartan|losartan]] in 1995, developed at the DuPont Merck laboratories from a series of imidazole leads first reported by Takeda chemistry.<ref name="carini1991">Carini DJ, Duncia JV, Aldrich PE, Chiu AT, Johnson AL, Pierce ME, Price WA, Santella JB 3rd, Wells GJ, Wexler RR, et al. Nonpeptide angiotensin II receptor antagonists: the discovery of a series of N-(biphenylylmethyl)imidazoles as potent, orally active antihypertensives. ''Journal of Medicinal Chemistry''. 1991 Aug;34(8):2525-2547. PMID 1875347.</ref>

The [[:Category:Calcium_channel_blockers|calcium channel blockers]] entered cardiovascular medicine through a separate door. [[Verapamil|Verapamil]], synthesized in Germany in 1962, was the first agent shown by [[wikipedia:Albrecht Fleckenstein|Albrecht Fleckenstein]] to block the slow inward calcium current of cardiac and vascular smooth muscle.<ref name="fleckenstein1983">Fleckenstein A. History of calcium antagonists. ''Circulation Research''. 1983 Feb;52(2 Pt 2):I3-16. PMID 6297830.</ref> [[Nifedipine|Nifedipine]] and the rest of the dihydropyridine family followed; [[Amlodipine|amlodipine]], with its long plasma half-life and gradual onset, provided in 1992 the once-daily dosing and freedom from reflex tachycardia that the immediate-release dihydropyridines had lacked. By the end of the twentieth century five medication classes, the diuretics, the ACE inhibitors, the angiotensin receptor blockers, the calcium channel blockers, and the beta-blockers, were established as the building blocks of essential-hypertension therapy.

The remaining clinical question, and it remains alive, is the treatment target. The early VA trials set a working aim of "below 140/90" by convention. The Hypertension Optimal Treatment trial in 1998 examined diastolic targets between 80 and 90 millimetres of mercury and could not show clear benefit of the lower one.<ref name="hot1998">Hansson L, Zanchetti A, Carruthers SG, Dahlöf B, Elmfeldt D, Julius S, Ménard J, Rahn KH, Wedel H, Westerling S, for the HOT Study Group. Effects of intensive blood-pressure lowering and low-dose aspirin in patients at high risk of cardiovascular disease: principal results of the Hypertension Optimal Treatment (HOT) randomised trial. ''Lancet''. 1998 Jun 13;351(9118):1755-1762. PMID 9635947.</ref> The Systolic Blood Pressure Intervention Trial in 2015, by contrast, randomized patients at high cardiovascular risk to a systolic target of 120 versus 140 and was stopped early for benefit in the intensive arm, at the cost of a higher rate of hypotension, syncope, and acute kidney injury.<ref name="sprint2015">SPRINT Research Group, Wright JT Jr, Williamson JD, Whelton PK, Snyder JK, Sink KM, Rocco MV, Reboussin DM, Rahman M, Oparil S, et al. A randomized trial of intensive versus standard blood-pressure control. ''New England Journal of Medicine''. 2015 Nov 26;373(22):2103-2116. PMID 26551272.</ref> Current American guidelines have settled, for most adults, on a treatment goal of less than 130/80 millimetres of mercury, while acknowledging that the evidence base for any single threshold remains contested and that the absolute benefit of treatment scales with the patient's baseline cardiovascular risk rather than with the blood pressure alone.<ref name="whelton2018">Whelton PK, Carey RM, Aronow WS, Casey DE Jr, Collins KJ, Dennison Himmelfarb C, DePalma SM, Gidding S, Jamerson KA, Jones DW, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults. ''Hypertension''. 2018 Jun;71(6):e13-e115. PMID 29133356.</ref>

== Classes indexed ==

The principal medication classes by which the arterial blood pressure is lowered in modern practice:

* [[:Category:ACE_inhibitors|Angiotensin-converting enzyme (ACE) inhibitors]]: [[Benazepril|benazepril]], [[Enalapril|enalapril]], [[Lisinopril|lisinopril]], [[Ramipril|ramipril]]
* [[:Category:Angiotensin_receptor_blockers|Angiotensin receptor blockers (ARBs)]]: [[Irbesartan|irbesartan]], [[Losartan|losartan]], [[Olmesartan|olmesartan]], [[Telmisartan|telmisartan]], [[Valsartan|valsartan]]
* [[:Category:Calcium_channel_blockers|Calcium channel blockers]] (dihydropyridine and non-dihydropyridine): [[Amlodipine|amlodipine]], [[Diltiazem|diltiazem]], [[Nifedipine|nifedipine]], [[Verapamil|verapamil]]
* [[:Category:Thiazide_diuretics|Thiazide diuretics]] and [[:Category:Thiazide-like_diuretics|thiazide-like diuretics]]: [[Hydrochlorothiazide|hydrochlorothiazide]], [[Chlorthalidone|chlorthalidone]]
* [[:Category:Alpha-1_blockers|Alpha-1 adrenergic blockers]] (where also used in prostatic hyperplasia): [[Doxazosin|doxazosin]], [[Terazosin|terazosin]]
* [[:Category:Direct_vasodilators|Direct arteriolar vasodilators]]: [[Hydralazine|hydralazine]]

Closely related classes whose principal indication is not hypertension but which lower blood pressure as part of their action are collected separately: the [[:Category:Beta-blockers|beta-adrenergic blockers]], the [[:Category:Aldosterone_antagonists|aldosterone antagonists]], the [[:Category:Loop_diuretics|loop diuretics]] when used in resistant hypertension or hypertension complicated by heart failure, and the centrally-acting sympatholytic agents ([[wikipedia:Methyldopa|methyldopa]], [[wikipedia:Clonidine|clonidine]], [[wikipedia:Reserpine|reserpine]]), the last three of which are now of largely historical interest.

== Notes on scope ==

The boundary of this category is "medicine whose principal or clinically important antihypertensive effect contributes to its place in prescribing." A medicine is listed here when blood-pressure lowering is one of its established indications, regardless of how it lowers the pressure. Some medicines listed here are also listed elsewhere because their principal indication is a different cardiovascular problem: the calcium channel blockers are antianginal as well as antihypertensive, the beta-blockers are antianginal and antiarrhythmic, the alpha-1 blockers are also used in benign prostatic hyperplasia. The multi-membership convention of this wiki permits a medicine to sit in every category that describes it. Hypertensive crises, managed with intravenous medicines in the acute setting ([[wikipedia:Sodium nitroprusside|sodium nitroprusside]], intravenous nicardipine, labetalol, esmolol, clevidipine), are within scope when those medicines have a dedicated page.

== About these pages ==

This category page is an encyclopedia article about its subject. The actual index of medicines belonging to the category is generated automatically by the wiki engine, from category-membership declarations on the individual medicine pages, and appears at the foot of the page below the references.

== References ==

<references/>

[[Category:Medicines]]
[[Category:Cardiovascular_agents]]
[[Category:CuratedCategoryPage]]