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

The contribution of autonomic nervous system activity to the cardiovascular effects of delta-9-tetrahydrocannabinol (THC) was evaluated in 4 normal subjects. The peak heart rate rise after THC was attenuated by atropine and by propranolol, and nearly abolished by atropine-propranolol pretreatment. Blocking drugs also attenuated THC-induced changes in forearm blood flow and vascular resistance but did not affect changes in fingertip temperature. The data suggest that THC acts to induce sympathetic stimulation and parasympathetic inhibition of cardiovascular control pathways. Cardiovascular responses in an additional subject who developed hypertension after either intravenous or smoked marijuana are described.
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PMID:Cardiovascular effects of intravenous delta-9-tetrahydrocannabinol: autonomic nervous mechanisms. 42 89

Acute experiments were conducted on cats; it was found that prostaglandine (PG) E1 produced a contrary effect on the tone of the cerebral vessels and on systemic arterial pressure depending on the presence of ethanol in its solution. Blocking of PG biosynthesis with indometacine promoted a marked increase in the vasoconstrictor reaction of the cerebral vessels and aided elevation of arterial pressure in response to noradrenaline administration. It is supposed that disturbance of PG biosynthesis in the organism could play a definite role in the genesis of hypertension and cerebrovascular disturbances.
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PMID:[ The effect of prostaglandin E1 and noradrenaline on the tone of cerebral vessels and arterial pressure]. 122 98

beta-Blocking therapy is used extensively is conditions as diverse as hypertension, angina pectoris, arrhythmias, thyrotoxicosis, hypertrophic cardiomyopathy, migraine, glaucoma, and myocardial infarction. Studies show they beneficially influence sinus node and atrioventricular conduction, but excessively high doses may cause sinus arrest or sinoatrial block. Nonselective beta-blockade in asthmatic patients may aggravate bronchoconstriction, whereas increased airways resistance is less likely with beta 1-selective, partial agonist, or alpha-beta-blocking drugs. Hypoglycemia can be prolonged; beta 1-selective or partial agonist drugs may cause less interference with glucose metabolism. beta-Blockade affects free fatty acids, lipids and lipoproteins, thyroid hormones, and parathormone. beta-Blockade may normalize abnormal platelet aggregation. Finally, the choice of the most effective drug depends on the clinician's knowledge of the various pharmacodynamic and pharmacokinetic drug profiles, allied with familiarity of the patient's medical condition.
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PMID:Circulatory and metabolic aspects of beta-adrenoceptor blockade. 290 49

1. Beta-Blockers are of similar efficacy in the treatment of hypertension to other antihypertensive drugs of first choice; they have a wide spectrum of activity both alone and in combination. 2. Although beta-blockers first appear to worsen the haemodynamic changes of hypertension, subsequently peripheral resistance falls. The cardiovascular reflexes responsible for the responses of posture or other responses requiring normal functioning of alpha-mediated tone are not inhibited. 3. Important contra-indications are asthma and heart failure in susceptible subjects. Lipid soluble drugs have somewhat greater CNS side effects. 4. Triglyceride levels, notably an increase in VLDL and a fall in HDL occur from non-selective agents (less so from beta 1-selective agents) and there is a marginal effect from drugs with relatively high ISA. 5. In contrast to other antihypertensive drugs beta-blockers reduce the myocardial infarction rate in high risk patients (i.e. post-myocardial infarct). Results in primary prevention of mild hypertension have been less promising. 6. Those drugs which are lipid soluble and liver metabolized result in greater variation of plasma concentration after oral administration and some pharmacokinetic drug interactions. Once daily administration is possible with many beta-blockers. 7. beta-Blocking drugs have an established and proven place in the treatment of hypertension.
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PMID:Risk-benefits of antihypertensive drugs--beta-blockers. 290 32

Verapamil, a known Ca++ antagonist, has vasodilator properties and is of use in the management of mild to moderate hypertension. It is also known to possess PGE2 antagonistic properties and thus may enhance prostacyclin synthesis of action in the vascular endothelial cells. This may contribute to its antihypertensive action. Blocking of endogenous synthesis of prostaglandins by acetyl salicylic acid reversed the beneficial effect of verapamil in hypertensive patients. This supports the concept that the vasodilator and anti-hypertensive properties of verapamil are mediated in part by the modulation of prostaglandin system.
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PMID:Modification of anti-hypertensive action of verapamil by inhibition of endogenous prostaglandin synthesis. 695 24

Through the multiple actions of angiotensin II (AII), the renin-angiotensin system (RAS) participates in cardiovascular homeostasis. Angiotensin II acts by binding to specific membrane-bound receptors, which are coupled to one of several signal transduction pathways. These AII receptors exhibit heterogeneity, represented by AT1 and AT2 receptor subtypes. The AT1 receptor mediates the major cardiovascular action of the RAS. This receptor has been cloned from multiple species, disclosing features consistent with a transmembrane, G-protein-linked receptor. Further AII receptor heterogeneity is evident by the cloning of isotypes of the AT1 receptor. Blocking the interaction of AII with its receptor is the most direct site to inhibit the actions of the RAS. Many AII receptor antagonists, including peptide analogs of AII and antibodies directed against AII, possess unfavorable properties that have limited their clinical utility. The discovery and further development of imidazole compounds with AII antagonist properties and favorable characteristics, however, has promise for clinical utility. The leader in this field is a selective AT1 receptor antagonist losartan (previously known as DuP 753 or MK-954). Losartan was demonstrated to be an effective antagonist of many AII-induced actions and an effective antihypertensive agent in many animal models of hypertension (HTN). Losartan also demonstrated secondary benefits in preventing stroke, treating congestive heart failure (CHF), and delaying the progression of renal disease in animal models. Clinical studies confirm the AII antagonist action of losartan and suggest that losartan will be effective in the treatment of essential HTN. AII antagonism is likely to provide useful treatment in essential HTN and CHF, conditions in which the RAS is known to play a major role. The utility of AII antagonism may extend beyond that of HTN and CHF, as suggested by the potential usefulness of angiotensin-converting enzyme (ACE) inhibition in the treatment or prevention of many other diseases. The key advantage AII antagonists provide over ACE inhibitors is that they may avoid unwanted side effects, related to bradykinin potentiation with the latter drugs. The AII antagonists will help determine the role of the RAS in physiologic regulation and in the pathophysiology of various disease states.
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PMID:Angiotensin II receptor blockade: an innovative approach to cardiovascular pharmacotherapy. 830 Aug 85

Craniotomy for resection of cerebral arterial venous malformation has been associated with postoperative hypertension, which necessitates administration of large doses of antihypertensive medications to control blood pressure. Controlling blood pressure is essential because hypertensive episodes can lead to postoperative cerebral hemorrhage with increases in morbidity and mortality. We measured vasoactive peptide and catecholamine release in 13 patients who underwent resection of an arterial venous malformation and in a control group of 6 patients who presented for clipping of unruptured cerebral aneurysms. Plasma renin activity, angiotensin I and II, vasopressin, aldosterone, epinephrine, and norepinephrine levels were measured intraoperatively and for 36 h postoperatively. Analysis of variance was used to assess sample and group effects. A significant interaction between sample and groups was found for norepinephrine (p < 0.001) and renin (p = 0.002). Our data suggest that elevated plasma renin and norepinephrine levels are in part responsible for postoperative hypertension in patients undergoing resection of arterial venous malformations. Blocking the release of these hormones may help control blood pressure after surgery for removal of arterial venous malformations.
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PMID:Analysis of catecholamine and vasoactive peptide release in intracranial arterial venous malformations. 882 55

We evaluated the role of endogenous angiotensin II and III (ANG II and ANG III) at the rostral nucleus reticularis ventrolateralis (NRVL) in the modulation of baroreceptor reflex (BRR) response and the subtype of angiotensin receptors involved in this process. Adult male Sprague-Dawley rats anesthetized and maintained with pentobarbital sodium were used. Exogenous application of ANG II or ANG III (10, 20, or 40 pmol) by bilateral microinjection into the NRVL significantly suppressed the BRR response to transient hypertension induced by phenylephrine (5 micrograms/kg i.v.). The suppressive effect of ANG II (20 pmol) was reversed by an equimolar dose (1.6 nmol) of its peptide antagonist, [Sar1, Ile8]ANG II, and the nonpeptide antagonists for AT1 and AT2 receptors, losartan and PD-123319, respectively. On the other hand, the inhibitory action of ANG III (20 pmol) was blunted by its peptide antagonist. [Ile7]ANG III or PD-123319, but not by losartan. Blocking the endogenous activity of the angiotensins by microinjection into the bilateral NRVL of [Sar1, Ile8]ANG II, [Ile7]ANG III, or PD-123319 elicited an appreciable enhancement of the BRR response, whereas losartan produced minimal effect. These results suggest that, under physiological conditions, both endogenous ANG II and ANG III may exert a tonic inhibitory modulation on the BRR response by acting selectively on the AT2 receptors at the NRVL.
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PMID:Involvement of AT2 receptors at NRVL in tonic baroreflex suppression by endogenous angiotensins. 917 87

While arterial hypertension and renal dysfunction are well recognized complications of renal irradiation, the mechanisms that trigger the development of these complications are unknown. Recently, it was reported that the endothelium is a major target in radiation injury. Because dysfunction of the endothelial cells may lead or contribute to the development of hypertension and renal dysfunction in radiation nephropathy, we tested the hypothesis that endothelium-dependent vasodilation is impaired in radiated kidneys prior to the onset of hypertension. To test this hypothesis, we used Long-Evans rats that had undergone left nephrectomy (3 weeks earlier) and irradiation (3000 r's) to the right kidney 8 days earlier (mean blood pressures in the irradiated rats were not different than in the controls). We then measured the changes in renal blood flow (RBF) induced by endothelium-dependent (acetylcholine and bradykinin) and -independent (nitroprusside, norepinephrine, and angiotensin II) vasoactive agents. We found that the increases in RBF induced by the endothelium-dependent but not independent vasodilators were markedly impaired in the irradiated kidneys. Blocking nitric oxide synthesis with nitro L-arginine methyl ester in sham rats mimicked the blunted responsiveness of the irradiated rats, whereas indomethacin (an inhibitor of prostaglandin synthesis) had no effect on either sham or irradiated rats. Finally, the RBF responses to the endothelium-independent vasoconstrictors, norepinephrine and angiotensin II, were not altered in the irradiated kidneys. These results suggest that renal irradiation causes endothelial dysfunction (prior to the onset of hypertension) but spares the vascular smooth muscle cells.
Hypertension 1997 Sep
PMID:Abnormal endothelium-dependent responses in early radiation nephropathy. 932 3

Diabetic nephropathy is the most common cause of end-stage renal disease (ESRD) in the United States, and accounts for 35% of all the patients with ESRD entering a dialysis program; 63% of patients with diabetic nephropathy have type II diabetes mellitus. Hypertension is a major risk factor for renal disease and is common in people with diabetes mellitus. Strategies for preventing the progression of renal failure in patients with diabetes mellitus include glycemic control, and control of blood pressure. Blocking the renin-angiotensin system (RAS) slows the progression of established diabetic nephropathy in type I diabetes mellitus, and inhibiting angiotensin II formation retards or impedes the progression from microalbuminuria to established diabetic nephropathy (macroproteinuria) in people with type I diabetes mellitus. The situation could be the same for people with type II diabetes mellitus. The ability of RAS blockade using irbesartan, an AT1 angiotensin II receptor antagonist, to slow the progression in renal failure has been compared with that of the calcium channel blocker amlodipine and placebo in a pilot study. The results suggest that blockade of the RAS, in this case with irbesartan, is at least equivalent to calcium channel blockers with respect to antihypertensive efficacy, but provides better renoprotective benefits.
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PMID:Renoprotection and renin-angiotensin system blockade in diabetes mellitus. 943 77


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