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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

About 10% of survivors of an acute myocardial infarction will die in the following year. Thereafter the risk declines but reinfarction is still an important cause of mortality and morbidity. The post infarction trials have clearly shown that the best proven agents to mitigate this toll are aspirin, beta adrenoceptor blockers, and verapamil (but not other calcium blockers, except diltiazem for non Q wave infarction). In the context of hypertension treatment these post infarction trials may have important lessons for drug selection and ancillary treatment since the majority of subjects will ultimately die of ischaemic heart disease. Although the newer agents such as ACE and renin inhibitors, newer calcium channel blockers and alpha blockers have many promising properties in terms of risk factor reduction, no convincing mortality data exists; it is needed. This review will deal with the known effects (both good and bad) of antihypertensive agents and will also review other drug strategies relevant to the hypertensive patient. It will also point out large areas of ignorance.
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PMID:The secondary prevention of myocardial infarction by drug treatment; excluding lipid lowering agents. 134 57

Meta-analysis of several large interventional trials in patients with mild to moderate hypertension has shown that coronary events are reduced to a much lesser extent than expected. One of the possible explanations for this are the metabolic side-effects of diuretics and betablockers used in these trials that may counteract their beneficial blood-pressure-lowering effect. Diuretics, especially thiazide, increase total cholesterol (+5%) and LDL-cholesterol (+10%), while betablockers decrease HDL-cholesterol (-5%) and increase triglycerides (+20%). Calcium antagonists and ACE-inhibitors do not affect lipids, and alpha-blockers have some beneficial effects. Regarding the carbohydrate metabolism, diuretics and betablockers decrease insulin sensitivity, increase plasma insulin, LDL-cholesterol, and triglycerides, and reduce HDL-cholesterol. Calcium channel blockers are neutral, while alpha-blockers and ACE-inhibitors improve glucose tolerance and reduce insulin resistance. To date, the clinical relevance of this side-effects is not known. Controlled, long-term trials in hypertensive patients with calcium channel blockers, ACE-inhibitors, and alpha-blockers are needed.
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PMID:[Antihypertensive therapy and modification of metabolic risk factors (glucose and lipid metabolism)]. 135 32

Hypertension increases the risk of reinfarction and sudden death in post-myocardial infarction (MI) patients. The same s true of coexisting left ventricular hypertrophy. Fortunately, these two risk factors may be modified by pharmacotherapy. In this article, Dr Boden describes the complementary use of beta blockers and selected calcium channel blockers for secondary prevention after acute MI, particularly in the subset of patients who also have hypertension.
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PMID:The post-myocardial infarction patient with hypertension. Long-term outcome. 135

Systemic arterial blood pressure (BP), renal blood flow (RBF), and renal vascular resistance (RVR) were followed for 3-4 wks during the progression of DOCA-salt hypertension in the conscious dog. Accompanying the gradual increase in BP was an increase in RBF; however, RVR was unchanged. The hypertension was totally reversed 5-7 days after cessation of DOCA-salt treatment, but the increase in RBF persisted, presumably as a result of renal hypertrophy. Renal adrenoceptor blockade with prazosin (6 dogs) and prazosin plus idazoxan (4 dogs) caused a comparable decrease in BP in the normotensive and DOCA-salt hypertensive dog; however, RVR was decreased only in the normotensive. Similar results were obtained during ganglionic blockade with hexamethonium. The i.v. infusion of diltiazem for 1 wk restored BP of the hypertensive dog to a normotensive level, and hexamethonium given i.v. had little further effect on either BP or RVR. These results suggest a non-neurogenically mediated mechanism of canine DOCA-salt hypertension that is susceptible to calcium channel blockade.
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PMID:Renal hemodynamics in canine DOCA-salt hypertension: effect of calcium channel blockade. 135 81

Aerobic exercise may prevent hypertension and reduce blood pressure and mortality in hypertensive patients and those at high risk for coronary artery disease. Supervised aerobic exercise at an intensity of 70% to 80% of maximal aerobic capacity is recommended to achieve cardiovascular conditioning and other health benefits. When antihypertensive drug therapy is required, physicians should choose an agent that has favorable secondary effects, including hemodynamic responses to exercise. The most favorable effects are achieved with calcium channel blockers, angiotensin-converting enzyme inhibitors, alpha blockers, and central alpha agonists. The effects of diuretics are less desirable, and beta blockers should be a last choice for hypertensive patients who are physically active.
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PMID:Exercise and hypertension. Maximizing the benefits in patients receiving drug therapy. 135 18

Hypertension in kidney transplant patients is a common complication that affects long-term patient and allograft survival. Although multifactorial in nature, at least two causes can be corrected by surgical or radiologic intervention--stenosis and native kidney-associated hypertension. Unfortunately, the current immunosuppressive agents have added to the problem of hypertension. Both prednisone and cyclosporine appear to aggravate posttransplant hypertension. Newer agents are on the horizon that may address this problem. Currently, physicians should consider the possibilities of correctable forms of hypertension. If none are indicated, medical therapy with renal vasodilating drugs such as calcium channel blockers or converting enzyme inhibitors or both along with diuretics are usually effective.
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PMID:Hypertension and kidney transplantation. 136 20

Research on antihypertensive drugs not only provides new information on presently used agents but also leads to the introduction of exciting new compounds. Several important clinical trials involving currently available drugs have been published recently. Angiotensin-converting enzyme inhibitors improved survival in patients with milder degrees of congestive heart failure, which indicates that they have become the cornerstone of treatment for this condition. Angiotensin-converting enzyme inhibitors delayed or prevented the development of diabetic proteinuria (> 200 micrograms/min) in a placebo-controlled randomized trial. Further, enalapril was more effective than metoprolol in reducing the rate of decline in renal function in patients with type I diabetes. Calcium channel blockers protected against acute renal failure in patients after renal transplantation in two separate studies. Calcium channel blockers were shown to promote natriuresis, with negative sodium balance the same as that associated with thiazide diuretics. The voltage-dependent calcium channel has been cloned, and the binding sites of the three classes of calcium channel blockers are now known. beta-Blockers and thiazide diuretics were the drug treatments in the Systolic Hypertension in the Elderly Program trial and in the Swedish Trial in Old Patients with Hypertension study (patients 65 to 85 years). In both investigations, stroke and cardiovascular events were significantly reduced by these conventional inexpensive agents. Clonidine was found to lower blood pressure primarily by its interaction with the imidazole receptor rather than the alpha 2 receptor. Elucidation of the imidazole receptor promises to shed light on physiologic mechanisms as well as lead to the introduction of new agents, such as moxonidine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:New classes of antihypertensive drugs and new findings with established agents. 136 36

In the present study, we examined the regulatory mechanisms of calcitonin gene-related peptide on norepinephrine release in rat hypothalamus. Calcitonin gene-related peptide inhibited the stimulation-evoked norepinephrine release from hypothalamic slices of Sprague-Dawley rats in a dose-dependent manner, although the peptide did not affect basal release of norepinephrine. The blockade of the alpha 2-adrenergic receptors by RX 781094 failed to modulate the inhibitory effects of calcitonin gene-related peptide on norepinephrine release. Pretreatment of slices with islet activating protein, a toxin that interferes with the coupling of the inhibitory receptors to adenylate cyclase, did not affect the suppression of norepinephrine release by calcitonin gene-related peptide. However, Bay K 8644, a dihydropyridine-sensitive calcium channel agonist, significantly reversed the inhibitory effects of calcitonin gene-related peptide on norepinephrine release. These results show that calcitonin gene-related peptide might inhibit norepinephrine release in rat hypothalamus, partially mediated by interactions with dihydropyridine-sensitive Ca2+ channels but not by interactions with presynaptic alpha 2-adrenergic receptors and inhibitory guanosine triphosphate binding proteins. Furthermore, the finding suggests the possible involvement of calcitonin gene-related peptide in the regulation of sympathetic nervous activity in the central nervous system.
Hypertension 1992 Jun
PMID:Calcitonin gene-related peptide in noradrenergic transmission in rat hypothalamus. 137 86

Calcium channel antagonists, when used to treat hypertension, may modulate baroreflex function and vascular responsiveness to endogenous vasoconstrictors. We studied regional blood flow, cardiopulmonary baroreflex function, and pressor responses in nine hypertensive patients (mean age of 44 +/- 7 years), eight males and one female, treated with isradipine (ISR), a dihydropyridine calcium channel antagonist, in a placebo-controlled, crossover trial. Each patient underwent determination of blood pressure and forearm, splanchnic, and renal blood flows (by strain gauge plethysmography and indocyanine green and p-aminohippurate clearances, respectively) at baseline and during cardiopulmonary unloading by lower body negative pressure (LBNP) at -10 and -20 mm Hg. ISR decreased the mean arterial pressure from 105 +/- 2 to 93 +/- 2 mm Hg (p less than 0.01). ISR did not change supine forearm or splanchnic vascular resistances, but renal vascular resistance fell 30% during treatment (from 0.12 +/- 0.02 to 0.09 +/- 0.01 mm Hg min/ml, p less than 0.05). Cardiopulmonary baroreceptor unloading by LBNP elicited comparable effects on forearm, splanchnic, and renal vascular resistance before and during ISR treatment. Baroreceptor unloading during placebo did not change plasma NE or PRA; during ISR, LBNP elicited a progressive rise in these hormones. The pressor response to NE was potentiated during ISR treatment (p less than 0.05); in contrast, the pressor response to angiotensin II infusion was blunted by calcium blockade (p less than 0.05). The present study, therefore, demonstrates that calcium channel blockade with ISR preserves, and may even augment, cardiopulmonary baroreflex function. These physiologic responses may contribute to the relatively low incidence of symptomatic orthostatic hypotension observed during chronic treatment with this agent.
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PMID:Effect of isradipine on cardiopulmonary baroreflex function, regional blood flow, and vascular responsiveness in hypertensive patients. 137 97

Enhanced contractile responsiveness to the calcium channel agonist Bay K 8644 has been documented in large conduit arteries and small muscular arteries from hypertensive rats. The present study examined the effects of Bay K 8644 on the intracellular calcium concentration ([Ca2+]i) in microvessels from stroke-prone spontaneously hypertensive rats and normotensive Wistar-Kyoto rats. Using microspectrofluorometry of fura-2, [Ca2+]i was measured in smooth muscle cells localized on arteriolar fragments (15-35 microns external diameter) isolated after collagenase digestion of the pancreas. Resting [Ca2+]i in hypertensive arterioles (94 +/- 6 nM, n = 29) did not differ from that in normotensive vessels (81 +/- 4 nM, n = 40). KCl (50 mM), applied alone and in the presence of Bay K 8644 (30 nM), stimulated increases in [Ca2+]i that were reversed in calcium-free solution and with nifedipine (10 microM), consistent with activation of potential-operated calcium channels. Potassium-induced calcium transients were consistently potentiated by Bay K 8644. The change in [Ca2+]i evoked by KCl alone or in combination with Bay K 8644 did not differ between arterioles from hypertensive and normotensive rats. In 24% of the vessels from hypertensive rats and in 29% of those from normotensive rats, Bay K 8644 evoked an increase in [Ca2+]i that did not differ significantly between the two strains. The findings indicate that, in contrast to observations made in larger arteries, there is no evidence of a functional abnormality in potential-operated calcium channels in very small arterioles from genetically hypertensive rats.
Hypertension 1992 Sep
PMID:Calcium channel activation in arterioles from genetically hypertensive rats. 138 37


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