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

A 21 year old male was discovered to be severely hypertensive. He was found to have bilateral adrenal phaeochromocytomas and a single renal artery stenosis. More than 40 cases of coexisting renal artery stenosis and phaeochromocytomas have been reported. The aetiology of renal artery stenosis in association with phaeochromocytoma maybe multifactorial and the radiographic appearances are not always clear-cut. Renin levels in this patient were elevated prior to the removal of the phaeochromocytomas but the renal vein renin ratio did not suggest that the renal artery stenosis contributed significantly to his hypertension. The patient's hypertension resolved following successful removal of the phaeochromocytomas despite persistence of the renal artery stenosis. Thus, though renin levels may be misleading in these cases, renal vein renin ratios may still be helpful in deciding on patient management.
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PMID:Bilateral adrenal phaeochromocytomas associated with unilateral renal artery stenosis. 269 47

Previously we reported that immunoreactive angiotensin II (Ang II) release from isolated perfused rat mesenteric arteries was mediated by beta-adrenergic receptor activation. However, the precise mechanism of regulation of vascular renin-angiotensin is not completely understood. In this study, we examined the effect of indomethacin and meclofenamate on immunoreactive angiotensin I (Ang I) and immunoreactive Ang II release from perfused rat hind leg vasculature to delineate the possible relevance of prostaglandins to the vascular renin-angiotensin system in vitro. We also examined the effects of isoproterenol and propranolol on the immunoreactive Ang I and II release. Isolated rat hind legs were perfused with Krebs-Ringer solution, and immunoreactive Ang I and II released into the perfusate were measured directly by using a Sep-Pak C18 cartridge connected to the perfusion system. Indomethacin and meclofenamate (10(-8) to 2 X 10(-6) M) added to the perfusion medium suppressed immunoreactive Ang I and II release to similar extents in a dose-dependent manner (p less than 0.001); the maximal percent inhibition of immunoreactive Ang II release evoked by these inhibitors (2 X 10(-6) M) was 60 +/- 6% (p less than 0.001) for indomethacin and 50 +/- 4% (p less than 0.001) for meclofenamate. Isoproterenol (10(-6) M) failed to cause a change in the release of both peptides, but propranolol (10(-6) M) slightly decreased the release of immunoreactive Ang I and II by 28 +/- 4% (p less than 0.001) and 32 +/- 4% (p less than 0.001), respectively. There was a highly significant positive correlation between the released amount of immunoreactive Ang I and that of immunoreactive Ang II altered by indomethacin (r = 0.91), meclofenamate (r = 0.94), or propranolol administration (r = 0.90). These results suggest that the renin-angiotensin in the hind legs is modulated by prostaglandins and that a difference exists in the beta-adrenergic receptor-mediated release of Ang II among diverse vascular beds.
Hypertension 1988 Jul
PMID:Suppression of angiotensin II release by prostaglandin synthesis inhibitors in hind legs. 284 Mar 95

The tone of arterial blood vessels is regulated by the catecholamines through their receptors on arterial smooth muscle cells (ASMC). beta 2-adrenergic receptors of ASMC mediate vasodilation through agonist mediated c-AMP production. Previous reports have described these receptors on freshly isolated blood vessels. This study demonstrates the presence of beta 2-adrenergic receptors on cultured rat ASMC and that these receptors are functional. beta-adrenergic receptor binding was measured using [3H]-dihydroalprenolol (DHA) binding to the membrane of cultured ASMC from normotensive Wistar-Kyoto rats. The ASMC beta-adrenergic receptors have a Kd of 0.56 +/- 0.16 nM and a Bmax of 57.2 +/- 21.7 fmol/mg protein. Competition binding studies revealed a much greater affinity of these receptors for epinephrine than norepinephrine, indicating the preponderance of a beta 2-adrenergic receptor subtype. Isoproterenol stimulation of cultured ASMC resulted in a 14 +/- 7 fold increase in intracellular c-AMP content of these cells indicating these receptors are functional. beta-adrenergic receptors of cultured ASMC provide an excellent system in which the association between hypertension and observed beta-adrenergic receptor differences can be further explored.
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PMID:Beta-adrenergic receptor binding characteristics and responsiveness in cultured Wistar-Kyoto rat arterial smooth muscle cells. 284 67

Patients with hypertension or ischemic heart disease are often treated with beta-adrenoceptor antagonists, yet the degree of beta-adrenoceptor blockade has rarely been studied in relation to anesthesia. We have constructed isoproterenol dose-response curves in four groups of patients under general anesthesia: group I, 27 elderly normotensive patients not receiving drugs; group II, 14 hypertensive patients treated with cardioselective beta-adrenoceptor antagonists; group III, 15 hypertensive patients receiving nonselective beta-adrenoceptor antagonists; group IV, 13 patients receiving an infusion of labetalol at 0.15 mg X kg-1 X hr-1. Geometric mean CD25, the dose of isoproterenol required to increase the heart rate by 25 beats/min was 4.4 micrograms (3.5-5.6, 95% confidence interval (CI) of the mean) in group I, and 27 micrograms (19-38, 95% CI), 39 micrograms (29-52, 95% CI), and 95 micrograms (62-147, 95% CI) in groups II, III, and IV, respectively. All differences were significant (P less than 0.01), except those between groups II and III (P less than 0.1). No signs of myocardial ischemia and only a few transient arrhythmias were observed. Isoproterenol dose-response curves are a safe means to assess the degree of beta-adrenoceptor blockade during anesthesia and the postoperative period.
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PMID:Assessment of beta-adrenoceptor blockade during anesthesia in humans: use of isoproterenol dose-response curves. 285 67

The pattern of cardiac beta-adrenergic receptor changes in different hypertrophy models varies according to the pathophysiology. In salt-sensitive Dahl rats, high dietary salt intake leads to a moderate degree of cardiac hypertrophy associated with increased numbers of cardiac beta-adrenergic receptors but unchanged affinity for agonists. Isoproterenol-stimulated cardiac adenylate cyclase is also higher in salt-loaded hypertensive rats without any change in basal or NaF-stimulated activities. In contrast, neither beta-adrenergic receptors nor adenylate cyclase activities are affected by variations in dietary salt in salt-resistant Dahl rats. The extent of isoproterenol-induced down regulation of beta-adrenergic receptors on isolated cardiac myocytes as well as the recovery from this down regulation is not significantly different in either strain of Dahl rats and is not influenced by dietary salt. The enhancement of beta-adrenergic pathways in salt-dependent genetic hypertension may be involved both in the initiation of cardiac hypertrophy and the preservation of contractile function.
Hypertension
PMID:Cardiac beta-adrenergic receptors in salt-dependent genetic hypertension. 299 64

The widespread use of beta-adrenoceptor antagonists against hypertension, angina pectoris and migraine or as a preventive treatment after myocardial infarction has encouraged us to investigate the effects of these drugs on platelet function. The aim of this study was to examine whether beta-blocking drugs interfere with platelet beta- adrenoceptors and whether this dependency is related to their selectivity for beta-adrenoceptor subtypes. Beta-adrenoceptor stimulation of human platelets with isoprenaline increased cyclic AMP (cAMP), which is known to inhibit platelet aggregation. Furthermore, our studies showed that cAMP formation in vitro was stimulated by non-selective and beta 2-selective agonists, but not by the predominant beta 1-agonist prenalterol. Isoprenaline- stimulated cAMP formation was blocked by the non- selective beta-adrenoceptor antagonists propranolol, timolol, and alprenolol, while the beta 1-selective antagonists atenolol and metoprolol had no influence on an isoprenaline-induced cAMP formation. Receptor binding studies using (3H)-dihydroalprenolol revealed an IC50 value for propranolol of 85 nM, while metoprolol only displaced the bound (3H)-dihydroalprenolol at far higher concentrations (IC50, 20 microM). We conclude that the human platelet beta-adrenoceptors are mainly of the beta 2- subtype and that beta-adrenoceptor antagonists, especially the non-selective antagonists interfere with platelet function assessed as platelet cAMP formation.
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PMID:Characterization of human platelet beta-adrenoceptors. 300 61

Renal cortical slices obtained from male New Zealand rabbits were used to investigate the role of adenosine in the regulation of renin release. Isoproterenol produced a significant (p less than 0.01), twofold to threefold increase in renin release, that was both dose-dependent and time-dependent. Addition of either the l-phenylisopropyl or the N6-ethylcarboxamido derivative of adenosine attenuated this stimulation at concentrations as low as 10(-9) M or 10(-8) M, respectively. Higher doses of d-phenylisopropyladenosine (10(-6) M) or adenosine (10(-5) M) were necessary to significantly reduce the beta-adrenergic response (p less than 0.01). Inhibition was absent in slices preincubated with 10(-5) M 8-phenyltheophylline, a concentration that had no effect on either basal or stimulated renin release. The site of inhibition appeared to be distal to beta-adrenergic and prostaglandin receptors since l-phenylisopropyladenosine (10(-8) M) blocked stimulation by selective beta-adrenergic receptor agonists, prenalterol (10(-6) M) or salbutamol (10(-5) M), and by prostaglandin E1. These data suggest that adenosine and its analogues inhibit renin release and that this inhibition may be mediated by a receptor-dependent action on a common point in the pathway leading to release.
Hypertension 1987 Jun
PMID:Inhibition of renin release by analogues of adenosine in rabbit renal cortical slices. 303 78

Previous studies suggested that left ventricle papillary muscles from neurogenic hypertensive rats with 15 days of sino-aortic denervation (SAD) develop intense depression of their inotropic state. Considering that these animals have an increased cardiac sympathetic tonus that could produce the observed depression of the contractile response we did the present study simulating a cardiac sympathetic hyperactivity pretreating rats, during 15 days, with isoproterenol (IPA, 0.1 mg/kg, i.p., divided in 3 daily doses). Because SAD rats also develop hypertension, the effect of blood pressure overload was studied in rats with 15 days of renovascular hypertension (RHR), Goldblatt 1K1C, to compare, separated, the effects of sympathetic hyperactivity and hemodynamic overload. Results showed that RHR had muscles that developed larger force than their controls (C: 7.31 +/- 0.34 g/mm2, RHR: 12.8 +/- 0.40 g/mm2), meanwhile IPA pretreated rats had muscles developing less force than their respective controls (C: 13.8 +/- 0.37 g/mm2, IPA: 8.61 +/- 0.24 g/mm2). These results are according to the proposition that the contractile state depression is related to the sympathetic hyperactivity, as suggested by the IPA pre-treated group and because the animals with isolated pressure overload showed a better contractile performance when compared to their uninephrectomized controls.
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PMID:Contractile performance of papillary muscles of renovascular hypertensive and isoproterenol-pretreated rats. 337 90

The drinking response to systemic injection of isoprenaline has been used to study the decreased beta-adrenergic reactivity in hypothyroid rats. Using the same test, the beta-adrenergic responsiveness has been investigated in two models of experimental hypertension (DOCA-salt and Goldblatt two kidney one clip rats). Three weeks after induction of hypertension, control and hypertensive rats were injected subcutaneously isoprenaline (0.1 mg/kg) and the accumulative water intake at 1st, 2nd and 3rd hours was recorded. Isoprenaline induced a smaller drinking response in DOCA-salt hypertensive (DS) and DOCA-normotensive (D) rats than in normotensive (age control, normal uninefrectomized-salt and sham operated) or hypertensive Goldblatt two kidney one clip rats. Isoprenaline induced a 50% mortality in the mineral-corticoid treated D and DS rats. The present study suggests that the reduced beta-adrenergic response (water intake) and the rate of mortality observed in DOCA treated rats may be due to the absence of renin release after isoprenaline injection, as previously reported by us.
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PMID:[Water intake induced by isoprenaline in 2 models of experimental hypertension in rats]. 344 5

This study investigated vascular responsiveness in stroke-prone spontaneously hypertensive rats (SHRSP) and the effect of antihypertensive treatment on this responsiveness. Weanling (4-week-old) male and female SHRSP and Wistar-Kyoto rats (WKY) received either the antihypertensive combination treatment of hydralazine plus hydrochlorothiazide in drinking water or tap water alone (controls) for 15 weeks. Whereas the antihypertensive combination prevented the development of hypertension in treated SHRSP (SHRSP-T), blood pressure remained unchanged in treated WKY (WKY-T). Femoral arterial smooth muscle responsiveness to KCl, norepinephrine, and calcium (in the presence of either 40 mM KCl or 1 microM norepinephrine) was not altered in SHRSP when compared with WKY. A significant increase in the sensitivity of femoral arteries to KCl and calcium (in the presence of 40 mM KCl) was seen, however, in SHRSP-T and WKY-T. An increased sensitivity to norepinephrine and calcium (in the presence of 1 microM norepinephrine) was seen only in SHRSP-T. Isoproterenol-induced relaxation was significantly attenuated in both SHRSP and SHRSP-T. Relaxation induced by sodium nitroprusside and calcium (membrane stabilization) was not different between the four groups. These results show that femoral arterial smooth muscle responsiveness to vasoconstrictor stimuli is not altered in SHRSP but that beta-adrenergic-mediated relaxation is attenuated. Antihypertensive treatment resulted in an enhanced responsiveness to these vasoconstrictor stimuli but had no effect on the relaxation properties of femoral arterial smooth muscle.
Hypertension 1987 May
PMID:Vascular reactivity in the spontaneously hypertensive stroke-prone rat. Effect of antihypertensive treatment. 357 Apr 24


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