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

Saralasin (Sar1, Ala8 angiotensin II), a competitive antagonist of angiotensin II, or captopril, an angiotensin-converting enzyme inhibitor, were infused for 12 hr into conscious rats with Goldblatt two-kidney one-clip hypertension at an early stage (mean interval from clipping 36 days) and a chronic stage (151 days). In the early phase infusions of either saralasin or captopril produced a significant fall in blood pressure, which was maximal at 30 min, although the majority of animals remained hypertensive. In the chronic phase, saralasin produced a small and nonsignificant fall in blood pressure, whereas captopril produced a fall similar to that observed in the early group. No further fall in blood pressure was seen over the 12 hr period. PRC was markedly elevated in the early phase but did not differ significantly from normal in the chronic phase. The blood pressure fall produced by saralasin was significantly correlated with preinfusion PRC (r = 0.72 for the early group and 0.81 for the chronic group; p less than 0.01), whereas the fall in blood pressure produced by captopril was poorly correlated with PRC (r = 0.04 and 0.14, respectively). Captopril produced a minor fall and saralasin a minor elevation of blood 3 pressure in normal animals. Infusions of dextrose without inhibitor caused no change in blood pressure. Removal of the renal artery clip normalized blood pressure in the majority (88%) of animals in either the early or chronic phases. It is concluded that 12 hr infusions of these inhibitors are no more effective than 30 min infusions and do not fully correct hypertension in this model. Furthermore, the greater vasodepressor effect of captopril compared to saralasin in chronic hypertensive animals and the lack of correlation between PRC and change in blood pressure with captopril suggest that this agent has an action independent from blockade of the renin-angiotensin system. Removal of the renal artery clip is more effective than renin-angiotensin blockade in correcting Goldblatt two-kidney one-clip hypertension.
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PMID:Effect of 12-hour infusions of saralasin or captopril on blood pressure in hypertensive conscious rats. Relationship to plasma renin, duration of hypertension, and effect of unclipping. 701 68

The effect of acute hypercalcemia on blood pressure, blood volume, hemodynamic parameters, plasma norepinephrine, epinephrine, dopamine, renin, and aldosterone concentrations was investigated. After 1 hour of equilibration, 10 patients received an infusion of calcium gluconate in 5% dextrose (calcium 15 mg/kg of body wt in 3 hours). The calcium infusion increased the mean serum calcium from 8.7 to 13.0 mg/dl, the systolic blood pressure from 144 +/- 10 to 184 +/- (SEM) 12 mm Hg (P less than 0.001), the diastolic pressure from 78 +/- 4 to 93 +/- 5 mm Hg (P less than 0.01). The plasma volume was decreased by 9% (P less than 0.001), whereas the hematocrit was increased (P less than 0.05). Heart rate and cardiac output remained unchanged. Total peripheral resistance was increased from 1643 +/- 223 to 2256 +/- 387 dyne.sec/cm5 (P less than 0.05). The plasma epinephrine concentration rose from 4.5 +/- 0.7 to 6.9 +/- 1.2 ng/dl (P less than 0.01). The plasma norepinephrine concentration was unchanged after 2 hours and increased only slightly after 3 hours of calcium infusion. Plasma renin, aldosterone, and dopamine concentrations were not significantly changed. These findings demonstrate that acute hypercalcemic hypertension is mediated by an increase in peripheral vascular resistance. Hypercalcemic hypertension may be induced by a direct effect of calcium on blood vessels; calcium-mediated increase in adrenal epinephrine release may play a mild contributory role, and plasma volume contraction, an inhibitory role.
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PMID:Acute hypercalcemic hypertension in man: role of hemodynamics, catecholamines, and renin. 702 19

Conscious rats with two-kidney one clip Goldblatt hypertension had the constricting clip removed during continuous infusion of either dextrose, saralasin, or captopril. Other dextrose-infused animals underwent removal of the ischemic kidney or a sham procedure. Direct arterial blood pressure (BP) was recorded throughout the 15-hour preoperative and subsequent 24-hour postoperative period. Rats were studied in the "early" phase (1-3 weeks duration) or "chronic" phase (greater than 4 months) of hypertension. Animals subjected to a sham procedure returned to preoperative BP values. The BP of animals unclipped or nephrectomized did not return to previous hypertensive levels. Instead, a biphasic response was seen where BP partially recovered from an operative fall and then slowly declined to normal at 24 hours; this effect occurred in both stages of hypertension. At 24 hours, removal of the ischemic kidney was as effective as removal of the constricting clip in the correction of both early and chronic phase hypertension. Rats infused with saralasin or captopril demonstrated an acute (within 2 hours) and sustained fall in BP, but not to normotensive levels. This fall was significant in all animals (p less than 0.01) apart from chronic phase rats infused with saralasin where no significant fall was seen. Although animals infused with saralasin or captopril commenced at a lower preoperative BP, the biphasic pattern of response to unclipping was identical to that of dextrose-infused unclipped rats. Thus, sustained inhibition of the renin-angiotensin system did not modify the correction of hypertension produced by removal of the constricting clip, and the response to surgical correction did not appear to be entirely mediated by changes in the activity of the renin-angiotensin system, particularly in the chronic stage. Equally, the rapidity of correction is not consistent with a role of vascular hypertrophy.
Hypertension
PMID:Surgical reversal of two-kidney one clip hypertension during inhibition of the renin-angiotensin system. 703 35

In this study we used endothelin as a paradigm to explore the concept that some vasoactive agents, acting through mobilization of Ca2+ and stimulation of protein kinase C, can interact with human skeletal muscle and modify its glucose transport. Cultured human skeletal myoblasts from the vastus lateralis demonstrated two subclasses of high-affinity endothelin receptors and a robust increase in cytosolic free Ca2+ upon exposure to endothelin. The endothelin-evoked rise in cytosolic free Ca2+ primarily resulted from Ca2+ mobilization from intracellular organelles. Both endothelin and insulin enhanced [3H]deoxy-D-glucose uptake in human myoblasts, but their effects were not additive. These findings also were observed in differentiated myotubes of L6 skeletal muscle cells. Moreover, [3H]deoxy-D-glucose uptake in human myoblasts was enhanced by treatment with phorbol 12-myristate 13-acetate. The endothelin- and insulin-mediated increases in [3H]deoxy-D-glucose were totally ablated by treatment with calphostin C. Such observations suggest that endothelin can enhance glucose uptake in human skeletal muscle. This is mediated through mechanisms that are at least partially protein kinase C dependent. Thus, increased levels of endothelin in vascular beds may contribute to altered glucose metabolism in essential hypertension.
Hypertension 1994 Jun
PMID:Endothelin mobilizes calcium and enhances glucose uptake in cultured human skeletal myoblasts and L6 myotubes. 751 52

This study was undertaken to characterize blood pressure (by continuous blood pressure recording), renal hemodynamics, and excretory function in high-fructose-fed insulin-resistant dogs. We fed 10 mongrel dogs for 28 days with a normal sodium diet containing 60% of the calories either as fructose (n = 6) or dextrose (n = 4). Fructose-fed dogs developed insulin resistance by the 21st day of the experimental diet, as estimated by the mean glucose concentrations (in arbitrary units, AU) during the final hour of the insulin suppression test (640.3 +/- 57 AU fructose-fed dogs upsilon 397.5 +/- 24.7 AU dextrose fed dogs; P < .05). Neither of the groups showed any change in body weight, or in fasting plasma levels of glucose or insulin. There was no difference in mean arterial pressure between the groups before or during either diet, nor did we find any important alterations in renal function in these animals. We conclude that insulin resistance can be induced by a high-fructose diet in the dog. However, it is not accompanied by either hypertension or alteration in renal function. These findings emphasize the importance of continuously recording blood pressure under resting conditions and suggests that in the fructose-fed dog, insulin resistance does not appear to lead directly to hypertension.
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PMID:High-fructose feeding elicits insulin resistance without hypertension in normal mongrel dogs. 754

Fosinopril is distinguished from other ACE inhibitors by a pharmacokinetic pecularity in the sense that is can be metabolized either by liver or kidney. This was the rationale of the present research the aim of which was to verify if administered to patients with liver cirrhosis the drug was liable to alter global liver function and ability to metabolize drugs. Eight cirrhotic males, mean age 56 years, also suffering from high blood pressure, were studied. In these patients, liver and kidney function tests (BUN, creatinine blood level, serum and urinary electrolytes, creatinine clearance, calcium and phosphor blood level, transaminases, alkaline phosphatase prothrombin time, cholinesterase, gamma-glutamyl-transpeptidase) were carried out at baseline and after 30 days' fosinopril treatment (1 capsule every morning in the fasting state); in addition total functioning liver mass was assessed by the galactose test, and drug-metabolizing capacity by the antipyrine test. Treatment resulted in a significant improvement of pressure values in all patients (p < 0.01) and did not alter liver and kidney function parameters. Besides, no side effects were registered, especially no case of orthostatic hypotension. The antipyrine test was not influenced by fosinopril treatment. Therefore, short-term treatment with this ACE-inhibitor can be concluded to be effective and not to cause additional alterations of liver function in patients with liver cirrhosis.
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PMID:[Evaluation of the total hepatic function after treatment with fosinopril in hypertensive patients with liver cirrhosis]. 772 Mar 55

Hypertensive patients are heavier and have a more centralized body fat distribution, which is associated with risk factor clustering and resistance to insulin's actions, including suppression of plasma nonesterified fatty acids. We postulated that abnormalities of nonesterified fatty acids contribute to the increased vascular alpha-adrenergic reactivity and tone observed in our previous studies of obese hypertensive subjects. To test this hypothesis, in two separate protocols 10% Intralipid was infused into a dorsal hand vein with heparin to activate lipoprotein lipase and raise fatty acid levels locally. In protocol 1, the effects of Intralipid/heparin compared with those of 5% dextrose/heparin on dorsal hand vein sensitivity to phenylephrine were assessed by use of the linear variable differential transformer technique in 8 normotensive subjects. In protocol 2, the effects of Intralipid/heparin were compared with those of saline/heparin on hand vein responses to both phenylephrine and angiotensin II in 11 normotensive African American women. Intralipid/heparin reduced the dose of phenylephrine required to produce 50% of the maximal venoconstrictor response from 582 to 137 ng/min (compared with dextrose/heparin, P < .01) in protocol 1 and from 293 to 137 ng/min (compared with saline/heparin, P < .01) in protocol 2. Intralipid/heparin did not significantly alter hand vein responses to angiotensin compared with saline/heparin. These data suggest that abnormalities of nonesterified fatty acids in obese hypertensive patients with risk factor clustering may contribute to their increased neurovascular tone.
Hypertension 1995 Apr
PMID:Fatty acids enhance vascular alpha-adrenergic sensitivity. 772 31

We investigated the effect of raising arterial plasma epinephrine within the lower pathophysiological concentration range on various indicators of blood platelet function and hematocrit. Epinephrine was raised over 60 minutes by a stepwise increasing intravenous infusion in 40 healthy men aged 20 to 40 years. Platelet count increased progressively with increasing arterial epinephrine to a maximal change of 69 +/- 6 x 10(9)/L in EDTA-anticoagulated blood and a maximal change of 42 +/- 6 x 10(9)/L in acid-citrate-dextrose (ACD)-anticoagulated blood, and the weight of circulating platelets increased by 29% (P < .001). Platelet size increased significantly in EDTA and decreased in ACD, and the difference between EDTA and ACD was significant (P < .0001) for both count and size, suggesting that epinephrine not only recruits platelets into the circulation but also induces some microaggregation in vivo or adhesion ex vivo. Aggregation of platelets in vitro induced by epinephrine decreased (P < .003 for delta optical density and P = .038 for maximal optical density) after epinephrine infusion compared with saline but did not change when stimulated with ADP or collagen. These findings suggest a selective downregulation of the epinephrine-activating mechanisms concomitant with a rise in the platelet content of epinephrine by 81% (P < .001) and no change in the platelet sodium-proton membrane exchange. The release of granular content (beta-thromboglobulin and platelet factor 4) to the circulation in response to epinephrine was not significant. Thus, under acute conditions it seems that the platelets may protect themselves against inappropriate overstimulation by epinephrine. The importance of platelet epinephrine uptake is still unknown, but sodium-proton exchange does not seem to be involved in regulating the effects of circulating epinephrine on platelet function. Epinephrine has a pronounced effect on raising hematocrit (maximal change of 1.74 +/- 0.13 x 10(-2), P < .0001).
Hypertension 1995 May
PMID:Effect of circulating epinephrine on platelet function and hematocrit. 773 22

BACKGROUND AND METHODS. To determine the effects of hypertension on brain function, positron emission tomography (PET) studies using (18F)-2-fluoro-2-deoxy-D-glucose (FDG) were performed on a group of 17 otherwise healthy older hypertensive men (mean age +/- SD = 69 +/- 8 yr) and 25 age- and gender-matched controls. Subjects had medically treated essential hypertension for a minimum of 10 years (range = 10 to 24 yr) with no evidence of end-organ impairment from hypertension by routine clinical screening and by history. All hypertensive and control subjects were determined to be cognitively normal by extensive neuropsychological testing. The hypertensive subjects previously had been reported to have lateral ventricle enlargement and left hemisphere brain atrophy by quantitative MRI. PET data were analyzed using t-tests to look at group differences.
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PMID:Brain metabolic function in older men with chronic essential hypertension. 774

The presence of reduced venous distensibility in obesity might have important hemodynamic effects and could indirectly implicate a role for metabolic factors in vascular control, because loading conditions are different in arterial and in venous vessels. Forearm blood flow and venous volume were measured plethysmographically in 58 subjects, including lean and obese hypertensives and normotensives. Venous volume at 30 mmHg (VV30) was decreased by both obesity and hypertension. This coincided with evidence for better preservation of central blood and stroke volumes with upright posture in obese than in lean subjects. Furthermore, obese hypertensives had lower VV30 than either lean hypertensives or obese normotensives. Postischemic forearm vascular resistance, a surrogate marker for structural luminal cross-sectional area, percent body fat, and fasting insulin each correlated independently with VV30 (P < 0.05) in multivariate analysis. Because nonesterified fatty acid levels are elevated in obese hypertensives and may have potent vascular effects, dorsal hand vein responses to coinfusion of Intralipid 10% and heparin to raise fatty acids locally were obtained in normal volunteers. The local infusion of Intralipid with heparin reduced hand vein distensibility, whereas dextrose and heparin did not (11 +/- 3% vs. 0 +/- 2%, respectively, P < 0.01). This study indicates that obesity and mild hypertension each reduce venous distensibility and that the coexistence of both conditions produces an even greater impairment in venous capacitance. The reduced venous distensibility in obesity appears to reflect structural as well as functional factors and to have systemic hemodynamic effects.
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PMID:Additive effects of obesity and hypertension to limit venous volume. 786 53


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