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

Although endothelium-derived prostaglandin I2 stimulates renin release, exogenous endothelium-derived relaxing factor (EDRF) can inhibit it. To characterize the role of EDRF as an endogenous regulator of renin release, we inhibited or stimulated its production in rat renal cortical slices in vitro. Renin concentration in the incubation medium was determined by radioimmunoassay for angiotensin I (Ang I) generation. NG-Monomethyl-L-arginine (LNMMA) (10(-4) M), which blocks EDRF formation, significantly enhanced basal renin release from kidney slices by more than 50% in control medium (40.0 +/- 14.3 ng Ang I/hr/mg/30 min; p less than 0.01) or in medium treated with 1.6 x 10(-5) M meclofenamate (50.8 +/- 8.4 ng Ang I; p less than 0.025). Isoproterenol (10(-5) M)-stimulated renin release (40.0 +/- 14.3 ng Ang I; p less than 0.02) was not modified by LNMMA; addition of L-arginine (10(-5) M), the precursor of EDRF, did not change basal but blocked isoproterenol stimulation of renin. Nitroprusside (10(-5) M) completely reversed melittin-stimulated renin release. Endothelin-1, an endothelium-derived vasoconstrictor, inhibits renin release and stimulates EDRF and prostaglandin synthesis. To determine whether any of the renin-inhibiting effect of endothelin-1 was due to its stimulation of EDRF, we compared the effect of endothelin-1 on cortical slices with and without EDRF inhibition. Endothelin-1 (10(-7) M) decreased renin by 36.7 +/- 10.9 ng Ang I (p less than 0.01) compared with controls, and the response was the same after either LNMMA or hemoglobin treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1992 Feb
PMID:Nonprostanoid endothelium-derived factors inhibit renin release. 173 97

In an earlier report we observed alterations in aortic smooth muscle alpha- and beta-adrenergic responsiveness in the Dahl rat. The present study was designed to define the time course of these changes and further characterize the alterations in this model of hypertension. Four-week-old male Dahl salt-sensitive (DS) rats were placed on either a normal (DSN) or high salt diet (8% NaCl; DSH). Aortic smooth muscle responsiveness was studied at 3 and 6 weeks of the dietary treatment. No differences were seen between the 2 groups in either the contractile response to KCl or the relaxation responses to sodium nitrite and acetylcholine. Isoproterenol-induced relaxation was significantly attenuated and contractile response to norepinephrine (NE) were enhanced at 3 weeks of treatment in DSH rats, however, no differences were seen between the 2 groups at 6 weeks. Since alterations were seen only at 3 weeks of treatment, aortic smooth muscle responsiveness to the specific alpha-agonists phenylephrine (alpha 1), guanfacine (alpha 2) and contractile responses to NE in the presence of propranolol were evaluated at three weeks. No differences were observed between the 2 groups with any of these treatments. Thus, it appears that the increased NE responsiveness seen in aortic smooth muscle of DSH rats during the developmental stage of the hypertension is the result of a decrease in beta-adrenergic responsiveness and not an increase in alpha-adrenergic responsiveness.
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PMID:Reduction in aortic smooth muscle beta-adrenergic responsiveness results in enhanced norepinephrine responsiveness in the Dahl salt-sensitive rat. 185 Jun 72

Torsades de pointes (TdP) is a life-threatening ventricular tachycardia that occurs in the setting of a prolonged QT interval and is most frequently related to administration of antiarrhythmic drugs. Patients with organic heart disease, with low serum electrolyte levels, with a previous episode of TdP and with bradycardia or baseline QT prolongation may be at increased risk of developing TdP. After initiation of a QT prolonging therapy, the dosage should be modified if the QT interval reaches 560-600 ms. Cessation of medication and immediate hospitalization are indicated in the presence of lightheadedness, syncope, or increased frequency and complexity of ventricular premature beats. The conventional therapy of TdP with isoproterenol or cardiac pacing, although usually effective, has certain disadvantages. Isoproterenol is contraindicated in patients with hypertension or ischemic heart disease, whereas institution of cardiac pacing requires skilled personnel and fluoroscopy. Recently, infusion of magnesium sulfate has been shown to abolish TdP both in the clinical and experimental setting. Compared with conventional therapy, magnesium sulfate has the advantage of safety and simplicity of its administration. In doubtful cases, if does not aggravate a ventricular tachycardia that is not TdP, as may occur with isoproterenol. This advantage and the prompt effectiveness of the drug in four clinical series, including 31 patients, support the use of magnesium sulfate as the first line of therapy for TdP.
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PMID:Torsades de pointes: prevention and therapy. 185 60

Previous studies from our laboratory, have demonstrated that 21 days after unclipping the decrease in arterial pressure (AP) was followed by a regression of cardiac hypertrophy (CH) and a normalization of contractile response to Isoproterenol (I) stimulation in two kidney one clip (2K1C) hypertension. The purpose in this study was to reexamine the effects of Alpha Methyl Dopa (AMD) treatment on AP, CH and cardiac response to I stimulation in this model. A total of 43 male rats, ten weeks old, were used. In 19 rats a silver clip was placed under ether anaesthesia in the left renal artery (clip group) (K). The remaining 24 animals constituted the control group (C). Twenty one days later, in 9 and in 17 animals from K and C groups, treatment with AMD 100 mg/kg/day per os was started and maintained during the three week-follow-up period (K alpha and C alpha groups). AP was measured twice a week by the tail cuff method and body weight was registered once a week. We defined hypertension when the systolic pressure was 150 mmHg or more. Three weeks after clipping and 21 days after treatment, in the clipped animals, simultaneously with matched controls (C alpha and K alpha) the cardiac response to Isoproterenol stimulation was studied. For this purpose, under pentobarbital anesthesia the carotid artery and the femoral artery and vein were cannulated in order to measure mean arterial pressure (MAP), left ventricular systolic pressure, heart rate (HR) and DP/DT+ Max in basal conditions and after I (0.001, 0.02, 0.04, 0.12 and 0.24 microgram/kg).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of alpha methyldopa on heart in renovascular hypertension]. 215 63

The association of HBV infection and glomerular damage was first reported by Combes et al in 1971, in a patient with nephrotic syndrome due to membranous glomerulopathy and chronic hepatitis B. Since, then, other glomerular diseases have been reported such as a) minimal changes nephropathy, b) IgA nephropathy, c) membranous-proliferative glomerulonephritis (MPGN), d) membranous, e) mesangial proliferative and f) lupus nephritis. All of them are associated with chronic hepatic disease and some of the following antigens: 1) HBsAg; 2) HBeAg; 3) HBcAg. These disorders are very frequent in Southeast Asia. Vertical transmission from mothers to fetuses may be important in maintaining the high carrier rate, and possibly plays a role in the development of glomerular damage. On the other hand, MPGN associated with HBsAg has rarely been reported and always with a favorable benign course. The present report describes interesting findings in a renal biopsy from a HBsAg and HBeAg carrier, who developed renal failure requiring hemodialysis. A 21 year old Korean man was admitted to the Hospital for nephrotic syndrome, microhematuria hypertension and renal failure. He had no previous history of blood transfusion, intravenous drug addiction, jaundice or liver disease. His father was HBsAg carrier with hepatic cirrhosis. An ultrasound examination showed normal renal size. Renal biopsy was performed and the patient received hemodialysis treatment. The specimen was processed for light microscopy, immunofluorescent studies and peroxidase-antiperoxidase technique. Frozen sections were studied by direct immunofluorescence for the identification of IgG, IgA, C1q, C3, fibrinogen and albumin. Paraffin sections stained by immunoperoxidase technique for HBsAg, using polyclonal monospecific rabbit anti-Human antisera (Dakopatts, Copenhagen).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Membranoproliferative glomerulonephritis with semilunar forms and massive deposits of IgA associated with HBsAg]. 229 14

Chronic daily administration of cilazapril (1 X 10 mg/kg/day p.o., from age 4 to 14 weeks) to young spontaneously hypertensive rats (SHR) prevented the development of hypertension. The antihypertensive effect of a single dose of cilazapril persisted greater than 24 h. Discontinuation of long-term treatment resulted in an increase of systolic arterial blood pressure (SAP) to control hypertensive levels within 4 days. Following 10 weeks of drug administration, comparative hemodynamic studies were carried out on age-matched (14 weeks) control SHR and cilazapril-treated SHR. Cilazapril-treated SHR had a significantly lower mean arterial blood pressure (MAP) and total peripheral vascular resistance than did control SHR. The antihypertensive effect of cilazapril was not associated with changes in heart rate (HR). The myocardial performance parameters, cardiac output, and stroke volume, were similar in treated and control SHR, suggesting that the antihypertensive effect of cilazapril following chronic administration to SHR is mainly due to a reduction in peripheral vascular resistance. Vasopressor responses to angiotensin I were significantly lower in cilazapril-treated SHR than in control SHR. By contrast, pressor responses to angiotensin II and a high dose of norepinephrine (1.0 microgram/kg i.v.) were significantly enhanced. Isoproterenol elicited a fall in blood pressure in both groups, the extent of which was dependent upon the magnitude of basal blood pressure levels. Chronic cilazapril treatment resulted in a reduction of heart weight, suggesting that the drug may prevent development of cardiac hypertrophy in SHR. Kidney and adrenal weights were unaffected by the chronic treatment. Specific renin activities (SRA) in tissues of SHR were increased by factors of 20 (plasma) or 2 (kidney and adrenal) following cilazapril administration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cilazapril prevents hypertension in spontaneously hypertensive rats. 242 85

After a 2-week placebo period, 30 men, aged 60 years (mean), with mild or moderate hypertension were randomly assigned to one of three treatment groups: pindolol, 10 mg b.i.d.; epanolol, 200 mg b.i.d.; and epanolol, 400 mg q.d. At the end of the placebo period and of 4 weeks of active treatment, heart rate, blood pressure, plasma renin activity (PRA), and nonepinephrine (NE) concentration of subgroups of subjects, were measured during isoproterenol infusion (30 ng/kg.min-1 for 15 min) and submaximal ergometric exercise (89 W, mean). Sitting heart rates were reduced with 200 mg b.i.d. epanolol (p less than 0.01) but unchanged with pindolol and 400 mg q.d. epanolol. Reductions of systolic and diastolic blood pressures occurred in all treatment groups but were most pronounced with pindolol. Isoproterenol-induced cardioacceleration and rise in PRA and plasma NE concentration were abolished by pindolol but only attenuated by epanolol. Pindolol also abolished the isoproterenol-induced reduction in diastolic blood pressure; epanolol had no effect on it. The hemodynamic and hormonal responses to exercise were attenuated by pindolol and epanolol in proportion to their beta-blocking activities. In the doses used, epanolol had moderate beta 1-selective blocking action. The intrinsic sympathomimetic activity of epanolol is dose dependent.
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PMID:Antihypertensive and hormonal responses to beta-blockade with intrinsic sympathomimetic activity: pindolol versus epanolol. 244 3

The effects of atrial natriuretic factor (0.025 microgram/kg/min) on isoproterenol-(0.02 microgram/kg/min) and furosemide-(5 mg i.v. bolus) stimulated renin release were studied in seven salt-replete healthy volunteers. Isoproterenol or furosemide were given against a background infusion of 5% D-glucose (placebo day) or atrial natriuretic factor (experimental day). Atrial natriuretic factor abolished the rise in plasma renin activity caused by isoproterenol (p = 0.003) and significantly (p = 0.048) attenuated the rise in plasma renin activity after a bolus injection of furosemide. These results show that a pharmacological dose of atrial natriuretic factor inhibits stimulated renin release in humans. This attenuation is apparent with two heterogenous stimuli, which suggests a nonspecific effect.
Hypertension 1989 Jan
PMID:Atrial natriuretic factor inhibits isoproterenol- and furosemide-stimulated renin release in humans. 252 33

In 6 patients with untreated hypertension of mild or moderate degree, dilevalol was infused in the brachial artery. Doses were calculated to produce plasma levels approximating those achieved after oral dosing (0.03, 0.07, 0.1, 0.3 micrograms.kg-1.min-1) and also to produce plasma levels exceeding oral dosing (0.5, 1.0, 2.0 micrograms.kg-1.min-1) without causing any blood pressure or heart rate changes. The effects of the infusion on forearm blood flow were assessed by venous occlusion plethysmography. Dilevalol caused a progressive increase in flow in all subjects up to the intermediate dose given, with the effect being attenuated when the dose was increased further. Simultaneous propranolol infusion reduced the increase in flow induced by dilevalol, shifting the dilevalol-induced vasodilation dose response curve to the right. Isoproterenol infusion caused a marked, dose-related increase in flow that was equally well reduced by simultaneous infusion of dilevalol or propranolol. These results indicate that dilevalol effectively blocks peripheral vascular beta receptors in humans. The drug also acts as a partial beta 2-receptor agonist, causing vasodilation which can be reduced by co-administration of propranolol.
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PMID:Effects of dilevalol on forearm circulation in essential hypertension. 256 11

The direct effects of a renin inhibitor, N-acetyl-pepstatin and five angiotensin converting enzyme inhibitors, captopril and the active diacid forms of enalapril, ramipril, cilazapril, and CS-622, on the vascular renin-angiotensin system were examined in isolated perfused rat mesenteric arteries. Vascular renin activity and angiotensin II (Ang II) released into the perfusate were determined. Infusion of N-acetyl-pepstatin (5 X 10(-8)-5 X 10(-6) M) suppressed vascular renin activity and Ang II release dose dependently. Isoproterenol (10(-6) M) induced a 135 +/- 30% increase in Ang II release from the basal value. N-Acetyl-pepstatin (5 X 10(-6) M) suppressed isoproterenol-induced Ang II release. Infusions of 5 X 10(-6) M captopril and the diacid forms of enalapril, ramipril, cilazapril, and CS-622 by themselves had little effect on Ang II release, but concomitant infusion of isoproterenol with these angiotensin converting enzyme inhibitors significantly decreased Ang II release (71 +/- 21%, 51 +/- 40%, 8 +/- 21%, 69 +/- 24%, and 44 +/- 29% increase, respectively, from the basal values). These results indicate that N-acetyl-pepstatin suppresses the vascular renin-angiotensin system. This effect may in part contribute to the hypotensive actions of renin inhibitors. Although angiotensin converting enzyme inhibitors also suppress locally generated Ang II, the mechanism and physiological significance still remain to be clarified.
Hypertension 1989 Jun
PMID:Renin inhibitor and converting enzyme inhibitors suppress vascular angiotensin II. 266 30


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