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)

19-Nor-deoxycorticosterone (19-nor-DOC), a hypertensinogenic mineralocorticoid, equipotent with aldosterone and independent of the renin-angiotensin system, is synthesized in the kidney and excreted in excess in the urine of patients with aldosterone-producing adenomas. This current study evaluated the adrenal and renal venous levels of aldosterone and 19-nor-DOC after adrenal and renal venous catheterization and blood sampling in five patients with aldosterone-producing adenomas. Aldosterone (mean +/- SEM) in the adrenal vein ipsilateral to the tumor (469 +/- 293 ng/dl) was higher than in the contralateral vein (70 +/- 59 ng/dl). 19-Nor-DOC (mean +/- SEM) was also higher in the ipsilateral (548 +/- 286 ng/dl) than in the contralateral (51 +/- 14 ng/dl) adrenal vein. In the renal veins, ipsilateral aldosterone (2.2 +/- 0.8 ng/dl) and 19-nor-DOC (12.2 +/- 2.4 ng/dl) were respectively similar to contralateral aldosterone (1.5 +/- 0.5 ng/dl) and 19-nor-DOC (14.6 +/- 1.3 ng/dl), whereas 19-nor-DOC was higher than aldosterone in each renal vein. The present study demonstrates that 19-nor-DOC is produced, not only from the kidneys, but also from the ipsilateral adrenal of patients with aldosterone-producing adenomas. The ipsilateral adrenal 19-nor-DOC production is comparable to that of aldosterone, suggesting that 19-nor-DOC may be contributing to the hypertension and hypokalemia in this disease. In the contralateral adrenal, aldosterone is suppressed to a greater extent than 19-nor-DOC, suggesting that these two steroids are under the influence of two different regulatory mechanisms.
Hypertension 1992 Apr
PMID:19-Nor-deoxycorticosterone production from aldosterone-producing adenomas. 155 68

We studied the therapeutic efficacy of an intravenously injected antifibrotic agent encapsulated in liposomes on inhibiting collagen accumulation in hypertensive blood vessels. cis-4-Hydroxy-L-proline (cHyp) in liposomes was injected into rats exposed to 10% O2, and drug effect was evaluated by measuring right ventricular pressure and hydroxyproline content of the pulmonary artery. Right ventricular pressure was 11 +/- 1 mm Hg (mean +/- SEM) 5 days after a single intravenous injection of 200 mg/kg cHyp in liposomes compared with 14 +/- 1 mm Hg in rats injected with empty liposomes; hydroxyproline content was also reduced by cHyp treatment (87 +/- 6 versus 107 +/- 7 micrograms per vessel) (p less than 0.05 for both, n = 6-9). Injections of cHyp in liposomes every 5 days partially prevented hypertension and vascular collagen accumulation during a 3-week exposure to hypoxia, and the dose required was one tenth the dose of unencapsulated cHyp. Therapeutic doses of cHyp in liposomes injected for 6 months affected tensile properties of main pulmonary artery and aorta, but there were no apparent histological effects on other organs. Liposomes injected intravenously were identified in pulmonary artery endothelial cells. The prolonged effect of a single injection of cHyp in liposomes may be due to uptake of the liposomes by the endothelium. Liposome delivery of drugs to the arterial wall may be useful in the study and treatment of hypertensive vascular disease.
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PMID:Liposome-entrapped antifibrotic agent prevents collagen accumulation in hypertensive pulmonary arteries of rats. 156 1

The effect of renal vascular hypertension on blood pressure and plasma glucose, insulin, and triglyceride concentration was studied in Sprague-Dawley rats. Three weeks after the induction of renal artery sterosis, mean (+/- SEM) blood pressure was significantly greater (153 +/- 3 v 117 +/- 2 mm Hg, P less than .001) compared with that in sham-operated rats. However, the two groups were similar in terms of plasma glucose (140 +/- 3 v 140 +/- 2 mg/dL), insulin (27 +/- 3 v 23 +/- 2 microU/mL), and triglyceride (89 +/- 8 v 95 +/- 6 mg/dL) concentrations. Furthermore, blood pressure increased to a similar degree in the two groups of rats (22 +/- 4 v 24 +/- 2 mm Hg), as did plasma insulin (47 +/- 5 v 44 +/- 4 microU/mL) and triglyceride (407 +/- 50 v 381 +/- 46 mg/dL) concentrations, after 2 weeks of a high-fructose diet. These data indicate that experimental induction of renal vascular hypertension in normal rats was not associated with an increase in either plasma insulin or triglyceride concentration. Furthermore, the response of rats with renal vascular hypertension to a high-fructose diet was similar to that of the sham-operated group. These data support the view that hypertension, per se, does not lead to hyperinsulinemia and hypertriglyceridemia in normal rats.
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PMID:Renal vascular hypertension does not lead to hyperinsulinemia in Sprague-Dawley rats. 158 Oct 13

We have previously demonstrated that physiological hyperinsulinemia in normotensive humans increases sympathetic nerve activity but not arterial pressure since it also causes skeletal muscle vasodilation. However, in the presence of insulin resistance and/or hypertension, insulin may cause exaggerated sympathetic activation or impaired vasodilation and thus elevate arterial pressure. This study sought to determine if insulin causes a pressor response in borderline hypertensive humans by producing exaggerated increases in sympathetic neural outflow or impaired vasodilation. We recorded muscle sympathetic nerve activity (microneurography, peroneal nerve), forearm blood flow, heart rate, and blood pressure in 13 borderline hypertensive subjects during a 1-hour insulin infusion (38 microunits/m2/min) while holding blood glucose constant. Plasma insulin rose from 12 +/- 3 microunits/ml (mean +/- SEM) during control to 73 +/- 7 microunits/ml during insulin infusion and fell to 9 +/- 2 microunits/ml 2 hours after insulin infusion was stopped. Muscle sympathetic nerve activity, which averaged 25 +/- 2 bursts per minute in control, increased significantly during insulin infusion (+9 bursts per minute) and remained elevated 1.5 hours into recovery (+7 bursts per minute, p less than 0.001). Despite increased muscle sympathetic nerve activity, there were significant (p less than 0.001) increases in forearm blood flow and decreases in forearm vascular resistance during insulin infusion. Further, systolic and diastolic pressures fell approximately 3 and 6 mm Hg, respectively, during insulin infusion (p less than 0.01). This study suggests that acute physiological increases in plasma insulin elevate sympathetic neural outflow in borderline hypertensive humans but produce vasodilation and do not elevate arterial pressure.
Hypertension 1992 Jun
PMID:Insulin increases sympathetic activity but not blood pressure in borderline hypertensive humans. 159 58

The bradycardic response to baroreceptor stimulation is impaired in human and experimental hypertension. Because this bradycardia mainly depends on the vagus, this may reflect a reduced cardiac parasympathetic responsiveness, which would parallel the reduced cardiac adrenergic responsiveness observed in hypertension. To test this hypothesis, 12-week-old spontaneously hypertensive rats (n = 12) and normotensive Wistar-Kyoto rats (n = 11) were anesthetized with ketamine and underwent bilateral vagotomy. Cardiac parasympathetic responsiveness was assessed from the bradycardia induced by 1) graded electrical stimulation of the right efferent vagus (1-16 Hz) and 2) graded intravenous injections of methacholine (1-8 micrograms.kg-1). The slope of the linear regression between the bradycardiac response and the applied stimulus was taken as the measure of cardiac parasympathetic responsiveness. To identify the onset of possible alterations in cardiac parasympathetic responsiveness in hypertension, the study was extended to younger (8-week-old) spontaneously hypertensive (n = 11) and Wistar-Kyoto (n = 13) rats. With vagal stimulation, cardiac parasympathetic responsiveness was greater in 12-week-old spontaneously hypertensive rats than in 12-week-old Wistar-Kyoto rats (24.8 +/- 5.4 versus 10.1 +/- 1.2 beats per minute per hertz, mean +/- SEM, p less than 0.035). This was also the case with methacholine (18.8 +/- 3.5 versus 13.1 +/- 4.4 beats per minute per microgram per kilogram, p less than 0.045). In contrast, cardiac parasympathetic responsiveness was similar, with both vagal stimulation and methacholine, when tested in the younger spontaneously hypertensive and Wistar-Kyoto groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1992 Jun
PMID:Cardiac parasympathetic hyperresponsiveness in spontaneously hypertensive rats. 159 62

The local renin-angiotensin system may regulate adrenal cell growth and function. Angiotensinogen, renin, and angiotensin converting enzyme gene expression were studied in four normal adrenal glands (removed from patients with renal carcinomas) and five aldosterone-secreting adenomas. Northern blot analysis showed expression of angiotensinogen messenger RNA (mRNA) in normal adrenals at levels approximately 35-fold lower than liver and sixfold lower than kidney. Similar angiotensinogen mRNA levels were present in two aldosteronomas, whereas a third had levels approximately 50% of those found in kidney. Renin mRNA was detectable in most normal adrenals and in three adenomas, one of which had relatively high renin mRNA levels. Angiotensin converting enzyme gene was expressed in adrenal tissue and in three adenomas. Portions from these normal adrenals and two of these aldosteronomas, as well as samples from two other adrenals and three aldosteronomas, were also studied in an in vitro superfusion system coupled with active renin radioimmunometric assay, angiotensin II/III, and aldosterone radioimmunoassay. Total amounts of active renin and angiotensin II/III released from normal adrenals during 270 minutes of superfusion were higher than the amounts released from aldosteronomas (312 +/- 35 versus 187 +/- 43 and 823 +/- 100 versus 436 +/- 55 pg/100 mg tissue, respectively; mean +/- SEM, p less than 0.05), whereas aldosterone release from the adenomatous tissue was approximately threefold higher (320 +/- 21 versus 115 +/- 18 ng/100 mg tissue; mean +/- SEM, p less than 0.01). Total amounts of active renin and angiotensin II/III released by normal or adenomatous adrenal samples exceeded threefold to fourfold the amounts extracted from similar samples of the same surgical specimen.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1992 Jun
PMID:Local renin-angiotensin system in human adrenals and aldosteronomas. 159 71

We examined effects of a putative myosin light chain kinase inhibitor in the cerebral circulation in vivo. In anesthetized rats, diameter of basilar arteries was measured through a cranial window (control, 232 +/- 10 microns, mean +/- SEM). Vessel diameter was measured during topical application of agonists and antagonists. ML-7, which has been reported to compete with adenosine triphosphate for binding to the catalytic site on myosin light chain kinase, attenuated vasoconstriction in response to prostaglandin F2 alpha (10(-6) M; -22 +/- 1% before versus -14 +/- 1% and -3 +/- 2% during ML-7, 10(-7) and 10(-6) M, respectively; p less than 0.05). ML-7 (10(-6) M) did not affect baseline diameter. Responses to serotonin (10(-8) M) and phorbol 12,13-dibutyrate (10(-8) M) were not attenuated by ML-7. Thus, constriction of the basilar artery induced by prostaglandin F2 alpha in vivo is attenuated by an inhibitor of myosin light chain kinase.
Hypertension 1992 Jun
PMID:Signal transduction pathways in constriction of the basilar artery in vivo. 159 75

In untreated patients with uncomplicated essential hypertension, exercise induces an abnormal increase in blood pressure; the influences of this increase on exercise were evaluated by a cardiopulmonary exercise test (CPX) performed in control conditions (step 1) and during acute blood pressure reduction (step 2). Patients were classified as (1) normotensive (resting diastolic blood pressure [BPd] less than 90 mm Hg; n = 14), (2) mildly hypertensive (BPd of 90 to 104 mm Hg; n = 9), and (3) moderately to severely hypertensive (BPd greater than or equal to 105 mm Hg; n = 16). For the three groups, peak mean blood pressure during exercise was 125 +/- 5 mm Hg (mean +/- SEM), 144 +/- 3 mm Hg (p less than 0.01 vs normotensive), and 161 +/- 4 mm Hg (p less than 0.01 vs normotensive and p less than 0.01 vs mild hypertension), respectively. Oxygen consumption (VO2) at peak exercise and at ventilatory anaerobic threshold was 26.1 +/- 1.1 and 17.2 +/- 0.5 ml/min/kg, 25.4 +/- 1.1 and 16.9 +/- 0.8 ml/min/kg, and 26.4 +/- 1.3 and 17.5 +/- 1.2 ml/min/kg in normotensive subjects, those with mild hypertension, and those with moderate to severe hypertension, respectively. Fourteen normotensive subjects, six with mild hypertension, and nine with moderate to severe hypertension participated to step 2 (nifedipine vs placebo, double-blind crossover). Nifedipine reduced blood pressure at rest and at peak exercise in those with hypertension. Peak exercise VO2 was unaffected by nifedipine in both normotensive subjects and those with hypertension. With nifedipine, ventilatory anaerobic threshold occurred earlier and at a lower VO2 in mild and in moderate to severe hypertension (delta VO2 = -1.9 and -2.4 ml/min/kg, respectively). These findings might be due to nifedipine-induced redistribution of blood flow during exercise and might be the reason for the complaint of weakness after blood pressure reduction in hypertensive subjects.
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PMID:Exercise performance in patients with uncomplicated essential hypertension. Effects of nifedipine-induced acute blood pressure reduction. 160 Jul 77

The goal of this study was to investigate whether the elastic behavior of conduit arteries of humans or rats is altered as a result of concomitant hypertension. Forearm arterial cross-sectional compliance-pressure curves were determined noninvasively by means of a high precision ultrasonic echo-tracking device coupled to a photoplethysmograph (Finapres system) allowing simultaneous arterial diameter and finger blood pressure monitoring. Seventeen newly diagnosed hypertensive patients with a humeral blood pressure of 163/103 +/- 4.4/2.2 mm Hg (mean +/- SEM) and 17 age- and sex-matched normotensive controls with a humeral blood pressure of 121/77 +/- 3.2/1.9 mm Hg were included in the study. Compliance-pressure curves were also established at the carotid artery of 16-week-old anesthetized spontaneously hypertensive rats (n = 14) as well as Wistar-Kyoto normotensive animals (n = 15) using the same echo-tracking device. In these animals, intra-arterial pressure was monitored in the contralateral carotid artery. Mean blood pressures averaged 197 +/- 4 and 140 +/- 3 mm Hg in the hypertensive and normotensive rats, respectively. Despite the considerable differences in blood pressure, the diameter-pressure and cross-sectional compliance-pressure and distensibility-pressure curves were not different when hypertensive patients or animals were compared with their respective controls. These results suggest that the elastic behavior of a medium size muscular artery (radial) in humans and of an elastic artery (carotid) in rats is not necessarily altered by an increase in blood pressure.
Hypertension 1992 Jul
PMID:Conduit artery compliance and distensibility are not necessarily reduced in hypertension. 161 55

Hyperinsulinemia supposedly contributes to hypertension in diabetes mellitus. We sought to determine if the renal and cardiovascular effects of insulin are preserved in diabetes despite resistance to its glucose-lowering effect. We studied the effects of two doses of insulin (50 and 500 milliunits/kg.hr-1), using the euglycemic clamp technique, on fractional sodium excretion, blood pressure, and heart rate in two groups of non-insulin-dependent diabetics: eight patients with and eight patients without hypertension. Hypertensive diabetics had higher basal insulin levels than normotensive diabetics (21.8 +/- 2.9 and 14.4 +/- 1.6 milliunits/l, respectively [mean +/- SEM]; p = 0.03). The degree of insulin resistance, but not plasma insulin levels, correlated with the height of mean arterial blood pressure (r = 0.60 and 0.73 at the low and high insulin dose, respectively; p less than 0.05). In contrast, the change in mean arterial blood pressure correlated negatively with the change in endogenous insulin levels during the control experiment (r = -0.41, p less than 0.02). Exogenous insulin induced a similar reduction in fractional sodium excretion in normotensive and hypertensive diabetics (43 +/- 5.9% and 48 +/- 16.4% during the low insulin dose and 57 +/- 9.1% and 62 +/- 12.5% during the high insulin dose, respectively). A decline in blood pressure was noted that correlated with the whole body glucose uptake during the high insulin dose (r = 0.52, p less than 0.05). Since heart rate response and plasma norepinephrine level during the insulin clamp were comparable in both groups, an abnormality of the baroreceptor reflex is suggested. It appears that insulin resistance, but not insulin, is primarily related to hypertension. At the same time, insulin may still exert some effect on blood pressure by way of its renal or vasodilatory, or both, action.
Hypertension 1992 Aug
PMID:Acute hyperinsulinemia induces sodium retention and a blood pressure decline in diabetes mellitus. 163 61


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