Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of the present study was to compare influence of central arginine vasopressin (AVP) and of atrial natriuretic peptide (ANP) on control of arterial blood pressure (MAP) and heart rate (HR) in normotensive (WKY) and spontaneously hypertensive (SHR) rats. Three series of experiments were performed on 30 WKY and 30 SHR, chronically instrumented with guide tubes in the lateral ventricle (LV) and arterial and venous catheters. MAP and HR were monitored before and after i.v. injections of either vehicle or 1, 10 and 50 ng of AVP and 25, 125 and 500 ng of ANP. Sensitivity of cardiac component of baroreflex (CCB), expressed as a slope of the regression line was determined from relationships between systolic arterial pressure (SAP) and HR period (HRp) during phenylephrine (Phe)-induced hypertension and sodium nitroprusside (SN)-induced hypotension. CCB was measured before and after administration of either vehicle, AVP, ANP, or both peptides together. Increases of MAP occurred after LV administration of 1, 10 and 50 ng of AVP in WKY and of 10 and 50 ng in SHR. ANP did not cause significant changes in MAP in both strains as compared to vehicle, but it abolished AVP-induced MAP increase in WKY and SHR. CCB was reduced in WKY and SHR after LV administration of AVP during SN-induced hypotension. In SHR but not in WKY administration of ANP, AVP and ANP + AVP decreased CCB during Phe-induced MAP elevation. The results indicate that centrally applied AVP and ANP exert differential effects on blood pressure and baroreflex control of heart rate in WKY and SHR and suggest interaction of these two peptides in blood pressure regulation at the level of central nervous system.
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PMID:Central cardiovascular effects of AVP and ANP in normotensive and spontaneously hypertensive rats. 818 82

Patients undergoing kidney transplantation often suffer from essential hypertension and coronary artery disease, for which perioperative treatment with nifedipine proved to be effective. If calcium-channel blockers and nondepolarizing muscle relaxants are used simultaneously, their synergistic effect at the neuromuscular cleft must be considered. On the other hand because of its extrarenal elimination no significantly altered effects are expected for patients with terminal renal failure. This prospective study comprised 30 patients undergoing kidney transplantation who were 2 kg over normal weight after a preoperative dialysis and infusion of lactated Ringer solution. Fifteen minutes after introduction of balanced anaesthesia with isoflurane, nitrous oxide and fentanyl, patients were assigned to the treatment group (N) with hypertension (mean arterial pressure (MAP > 110 mmHg) and subsequent management with nifedipine or to the control group (0). Treatment was aimed at keeping MAP between 90 and 110 mmHg. The neuromuscular status was electromyographically assessed by the train-of-four-principle. There were evaluated the duration of action of the initial dose of atracurium (0.5 mg/kg) from injection time to T1 = 2% (WZ 2), the dose of atracurium for a continuous neuromuscular blockade (DD 98 in mg/kg/h), the recovery time and the recovery index. Fourteen patients with hypertension received a bolus of 10 micrograms/kg nifedipine. A significant reduction in blood pressure (p < 0.05) to the desired range was achieved by a subsequent infusion of nifedipine of 5 to 40 micrograms/kg/h. In 16 patients MAP was kept between 90 and 100 mmHg without any additional therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Anesthesia for renal transplantation: continuous neuromuscular blockade with atracurium and the management of intraoperative hypertension with nifedipine]. 824 Jun 42

2-(N-Propyl-N[(2'-[1H-tetrazol-5-yl]biphenyl-4yl)methyl]amin o) pyridine-3-carboxylic acid (ABBOTT-81988), a novel nonpeptide angiotensin II (AII) antagonist, was evaluated to characterize its antihypertensive activity in the conscious renal hypertensive rat. Oral or i.v. administration of ABBOTT-81988 at 0.03 to 0.3 mg/kg produced a dose-dependent, sustained decrease in mean arterial pressure (MAP; control 162-173 mm Hg, n = 27) of approximately 20 to 70 mm Hg. At a dose of 0.3 mg/kg p.o., ABBOTT-81988 lowered MAP to a normotensive level for more than 24 hr and did not change heart rate. During its antihypertensive effect (delta MAP, -28% approximately -35%), ABBOTT-81988 (0.1-03 mg/kg i.v.) decreased total peripheral resistance (delta resistance, -31% approximately -43%), and cardiac output remained either unchanged or slightly elevated. ABBOTT-81988 (0.3 mg/kg i.v.) produced an additional antihypertensive effect (delta MAP, -12 +/- 2%, n = 5) in captopril-pretreated (10 mg/kg i.v.) hypertensive rats, but captopril (10 mg/kg i.v.) had no effect in ABBOTT-81988-pretreated (0.3 mg/kg i.v.) rats. In the normotensive rat, ABBOTT-81988 (0.3 mg/kg p.o.) had no effect on basal MAP, but it inhibited the AII-induced (0.1 microgram/kg i.v.) pressor response by 51% to 91% for 24 hr, whereas the responses to norepinephrine (0.3 microgram/kg i.v.), vasopressin (0.03 IU/kg i.v.) and bradykinin (3 micrograms/kg i.v.) were not affected. It is concluded that ABBOTT-81988 is a safe and efficacious AII antagonist that may have use in the treatment of human hypertension.
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PMID:Characterization of antihypertensive activity of ABBOTT-81988, a nonpeptide angiotensin II antagonist in the renal hypertensive rat. 830 84

Although an increased prevalence of hypertension is associated with insulin-dependent diabetes, little is known about the effect of streptozotocin (STZ) diabetes on arterial pressure (AP) regulation in rats. Changes in AP induced by STZ, as well as associated factors in blood pressure regulation such as baroreflex sensitivity, plasma renin activity (PRA), plasma glucose and insulin levels and endothelium participation, were studied in male Wistar rats weighing 287 +/- 10 g. The same seven conscious rats were used for all measurements before and after STZ diabetes. AP pulses were stored on a videotape recorder and processed by a data acquisition system. Baroreflex sensitivity was evaluated by measuring heart rate (HR) changes induced by AP variations produced by phenylephrine and sodium nitroprusside injection. The effect of inhibition of nitric oxide synthesis with NG-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg i.v. bolus plus infusion at 20 mg kg-1 h-1) on AP was evaluated in another set of rats (6 normal and 5 submitted to STZ treatment). STZ induced hyperglycemia (306 +/- 19 mg/dl), a reduction in mean arterial pressure (MAP, from 116 +/- 5 to 101 +/- 4 mmHg) and no changes in HR (320 +/- 10 vs 298 +/- 14 bpm). The tachycardic response to arterial pressure decreases was impaired (-2.29 +/- 0.5 vs -4.5 +/- 0.7 bpm/mmHg, in control) while the bradycardic response to arterial pressure increases was unchanged. Pressure responsiveness to phenylephrine was impaired after STZ (3.78 +/- 0.4 vs 6.73 +/- 0.8 mmHg microU-1 ml-1, in control).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Streptozotocin diabetes modifies arterial pressure and baroreflex sensitivity in rats. 852 May 49

The present study was designed to investigate the role of cardiopulmonary reflex, more specifically the Bezold-Jarisch reflex, in experimental hypertension induced by chronic administration of Nw-nitro-L-arginine methyl ester (L-NAME) (0.5 mg/ml) added to the drinking water for 6 days. The study was performed in male Wistar rats (200-350 g), 9 animals per group. L-NAME ingestion caused a significant increase in resting mean arterial pressure (MAP: 182 +/- 4 mmHg) and heart rate (HR: 447 +/- 20 bpm) when compared to untreated rats (MAP: 112 +/- 3 mmHg and HR: 355 +/- 10 bpm). Cardiopulmonary receptors were chemically stimulated with bolus injections of 5-hydroxytryptamine (5-HT, 4-10 micrograms/kg, iv) followed by measuring the falls in diastolic arterial pressure (DAP) and HR in conscious and freely moving animals. As expected, the responses to intravenous injections of 5-HT consisted of a dose-dependent reduction in HR (from 26 +/- 14 to 175 +/- 25 bpm) and DAP (from 7 +/- 4 to 39 +/- 3 mmHg) in the control rats. Both bradycardia and diastolic hypotension were significantly accentuated in the L-NAME animals (approximately 30%). These data suggest that, in contrast to other models of hypertension, in the present one caused by inhibition of nitric oxide synthesis, the Bezold-Jarisch reflex is exaggerated. This neural dysfunction could be related to changes in the cardiac vagal efferent or effector.
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PMID:Exaggerated Bezold-Jarisch reflex in the hypertension induced by inhibition of nitric oxide synthesis. 858 Aug 77

Renal effects of FR139317, an endothelin ETA receptor antagonist, were examined using anesthetized normotensive and deoxycorticosterone acetate (DOCA)-salt hypertensive rats. The intravenous bolus injection of FR139317 (10 mg/kg) produced a slight decrease in mean blood pressure (MAP; -13%) in the control rats and this hypotension was accompanied by a moderate renal vasodilation (renal vascular resistance: RVR; -12%). In the DOCA-salt hypertensive rat, FR139317 had a more pronounced hypotensive effect (MAP; -26%) accompanied by a potent renal vasodilation (RVR; -33%). FR139317 significantly increased renal blood flow only in the DOCA-salt rats. In contrast, FR139317 produced a significant decrease in urine flow and urinary sodium excretion only in control rats. Northern blot analysis revealed that the renal prepro endothelin-1 (ET-1) mRNA level was significantly increased in DOCA-salt hypertensive rats. Thus, it seems likely that endogenous ET-1 is responsible for the maintenance of DOCA-salt-induced hypertension. We also suggest that at least in part, ET-1 and ETA receptors are involved in renal hemodynamic abnormalities in DOCA-salt-induced hypertension. The augmentation of renal ET-1 production may possibly have a function in the development and maintenance of DOCA-salt-induced hypertension.
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PMID:ETA receptor-mediated role of endothelin in the kidney of DOCA-salt hypertensive rats. 862 4

Activation of the sympathetic nervous system occurs in response to desflurane, causing tachycardia and hypertension. Fentanyl partially blunts the hemodynamic effects of desflurane but fails to attenuate the sympathetic response. This study determined the clinical effectiveness and dose response of alfentanil on the neurocirculatory responses to desflurane. Twenty-five healthy, male volunteers were randomized into one of three groups to receive either placebo (n = 9), 10 micrograms/kg intravenous (IV) bolus alfentanil (n = 9), or 20 micrograms/kg IV bolus alfentanil (n = 7) in conjunction with anesthetic induction by propofol, 2.5 mg/kg. Mean arterial pressure (MAP, radial artery), heart rate (HR), and efferent muscle sympathetic nerve activity (SNA, peroneal nerve) were recorded. After conscious baseline measurements, anesthesia was induced by propofol and alfentanil/placebo. One minute later, the desflurane vaporizer was activated at 11%. Neurocirculatory measurements were recorded for 11 min. There were no differences between the groups at conscious baseline. Induction of anesthesia was associated with significantly decreased MAP in the placebo and the 10 micrograms/kg alfentanil groups and increased HR in all groups with little change in SNA. In placebo subjects, desflurane administration increased HR and MAP above baseline. In both alfentanil groups, during desflurane administration HR and MAP never increased significantly above baseline. However, SNA was significantly increased in both groups. Alfentanil effectively blunts the hemodynamic changes but not the sympathetic responses associated with rapid increases in the inspired concentration of desflurane.
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PMID:Alfentanil modifies the neurocirculatory responses to desflurane. 871 95

Two groups of eight anesthetized dogs with pulmonary artery hypertension (PAH) were compared. PAH was induced by submitting one group (HP) to hypoxia (FiO2 range: 6-10%) and the other group (ME) to microemboli through glass microbead injection into the pulmonary circulation. Hypoxia-induced PAH was moderate (PAP: +65%; PVR: +152%) contrasting with marked PAH after microbead injection (PAP: +190%; PVR: +389%). For similar effects on left ventricular contractility (LV dP/dt max and segmental myocardial shortening), heart rate and systemic vascular resistance, left ventricular end-diastolic pressure showed significant differences between the two groups (HP group: +75%, ME group: -9%), and so did left ventricular end-diastolic length (HP: +9%, ME: -11%). Thus, contrary to the injection of microbeads, hypoxia did not give rise to any pulmonary barrier, and consequently the changes in cardiac output (HP: +19%, ME: -15%) and hepatic blood flow (HP: +383%, ME: -77%) were significantly different. Hypoxia, and not microbead injection, was responsible for systemic hypertension (MAP: +34% and -4%, respectively). The microbead model resulted in a significantly higher PVR/SVR ratio compared to the hypoxic model (HP: 0.14, ME: 0.41). Hypoxia increased left and right myocardial blood flows whereas microbead injection affected only right ventricular blood flow, leading to significantly different RV/LV endocardial perfusion ratios (HP: +10%, ME: +98%). We conclude that microbead-induced PAH is more appropriate than hypoxia-induced PAH for hemodynamic and pharmacological studies.
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PMID:Comparison between acute hypoxia-induced and mechanically-induced pulmonary artery hypertension on the hemodynamics, myocardial contractility and regional blood flow in dogs. 880 76

Our previous studies demonstrate that chronic insulin administration exacerbates hypertension in spontaneously hypertensive rats (SHR). In the present study, we tested the hypothesis that the pressor effect of insulin in SHR is medicated by sympathetic nervous system overactivity. Male SHR (7 weeks old) were given daily subcutaneous injection of insulin or vehicle for 3 days, after which each rat received an intravenous infusion of the peripheral ganglionic blocker hexamethonium. Two days later, in a second experiment, the infusion protocol was repeated with the alpha 2-adrenoceptor agonist clonidine, which more selectively inhibits sympathetic (as compared with parasympathetic) nervous system activity. Insulin treatment for 3 days caused a significant increase in mean arterial pressure (MAP; 164 +/- 2 mm Hg vs. saline control 148 +/- 3 mm Hg), but ganglionic blockade with hexamethonium eliminated the difference in blood pressure (BP) between the insulin-treated and control SHR. Infusion of clonidine significantly reduced MAP in the insulin-treated group to the level of the untreated control SHR, but the infusion did not reduce MAP in the latter group. In a second group of rats, acute administration of prazosin also eliminated the difference in MAP between insulin-treated and control SHR. We conclude that in SHR the sympathetic nervous system contributes importantly to the pressor effect of insulin administration and that this effect may be mediated by the central nervous system.
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PMID:Contribution of the sympathetic nervous system to hypertensive response to insulin excess in spontaneously hypertensive rats. 884 71

Hypertension and end-stage renal disease (ESRD) are major causes of morbidity and mortality in the United States, especially among African Americans. The African American Study of Kidney Disease and Hypertension (AASK) Pilot Study evaluated the feasibility of conducting a long-term clinical trial to compare the effects of two levels of blood pressure control and three different antihypertensive drug regimens on the rate of decline in glomerular filtration rate (GFR) in African Americans with clinically diagnosed hypertensive renal disease. African American men and women aged 18-70 years with a GFR of 25-70 ml/min/ 1.73m2 and hypertension were randomized in a 3 x 2 factorial design to initial treatment with either an angiotensin-converting enzyme inhibitor (enalapril), a calcium channel blocker (amlodipine), or a beta blocker (atenolol) and to a mean arterial blood pressure (goal MAP) of either 102-107 mm Hg or < or = 92 mm Hg. Furosemide, doxazosin, clonidine, hydralazine, and minoxidil were added sequentially until goal MAP was achieved. To compare the pathologic diagnosis with the clinical diagnosis of renal disease, study participants without contraindication were also asked to undergo a renal biopsy. The goals of the AASK Pilot Study were to evaluate recruitment techniques, adherence to prescribed antihypertensive drug regimens, ability of the antihypertensive regimens to achieve blood pressure goals, rates of participation in scheduled clinic visits and procedures, and variability of GFR measurements. A further goal was to obtain renal biopsy data in at least 75% of the randomized study participants. Compared to the ESRD patient population whose renal disease is caused by hypertension, women were underrepresented in the AASK Pilot Study. AASK Pilot Study participants had higher unemployment rates and lower income levels than African Americans in the general U.S. population.
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PMID:Design and baseline characteristics of participants in the African American Study of Kidney Disease and Hypertension (AASK) Pilot Study. 888 50


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