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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Essential hypertension (EH) can be subdivided according to the sympathetic and renin activity into two contrasting forms: (1) borderline beta-hyperadrenergic renin hyperresponsive and (2) stable beta-hypoadrenergic renin hyporesponsive EH. These two forms probably represent two expreme poles in the spectrum of EH in which sympathetic and renin hyper- or hyporeactivity cannot be accounted for by catecholamine determinations solely. beta-Adrenergic responsiveness monitored by plasma cyclic AMP determinations revealed plasma cyclic AMP, renin and circulatory hyperresponsiveness to isoproterenol in borderline hyperadrenergic EH while the opposite, cyclic AMP and renin hyporesponsiveness to insulin-induced hypoglycemia have been described in low renin stable EH. The kidney is in the center of the adrenergic abnormality in the two forms of EH with the borderline one excreting into the urine catecholamines not accounted for by their glomerular filtration. Catecholamines solely, however, do not account for the differences in both forms of EH which can probably be attributed to their different beta-adrenergic responsiveness.
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PMID:Catecholamines, cyclic AMP and renin in two contrasting forms of essential hypertension. 1 3

Insulin-induced hypoglycemia previously has been shown to provoke a beta-adrenergic response that normally results in an increase in plasma renin activity (PRA). In our study, hypoglycemia induced definite increases in PRA in a group of five patients with normal renin essential hypertension but failed to do so in a group of six patients with low renin essential hypertension. In both groups, plasma cyclic adenosine 3',5'-monophosphate (cyclic AMP; cAMP) increased more than 2-fold during hypoglycemia, but the response in the low renin group was significantly less than that previously observed in normal subjects under the same conditions. Plasma cortisol increased to an equal extent in both groups of hypertensive patients during hypoglycemia. Infusion of the phosphodiesterase inhibitor, theophylline, resulted in definite increases of PRA in patients with normal renin hypertension but not in patients with low renin hypertension. Because changes in the level of plasma cAMP during hypoglycemia have been thought to reflect adrenal catecholamine release, our finding of a blunted increase in plasma cAMP during hypoglycemia in patients with low renin hypertension may suggest that there is a generalized alteration in adrenergic responsiveness in this condition.
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PMID:Contrasting effects of hypoglycemia on plasma renin activity and cyclic adenosine 3',5'-monophosphate (cyclic AMP) in low renin and normal renin essential hypertension. 17 76

As plasma norepinephrine (NE) levels may be similar in hypertensive and normotensive subjects, the sensitivity of adrenergic receptors was investigated in patients with essential hypertension and normotensive subjects of similar age and sex. Alpha-adrenergic receptor sensitivity was measured in platelets by the specific binding of [3H]dihydroergocryptine and the NE inhibition of prostaglandin E1 (PGE1)-stimulated cyclic AMP (cAMP) production. The number of alpha-adrenergic receptors in platelets from hypertensive women was 1.5 times that in the platelets from normotensive ones, with no differences between hypertensive and normotensive women or between men and women in the affinity of the alpha-adrenergic receptor for [3H]dihydroergocryptine. PGE1-stimulated cAMP production was half as great in hypertensive as in normotensive men, while NE inhibition of PGE1-stimulated cAMP production was similar in hypertensive and normotensive men and women. [3H]Dihydroergoeryptine binding in female hypertensives, and PGE1-stimulated cAMP in male hypertensives did not differ from that in sex-matched controls. The sensitivity of the beta-adrenergic receptor, measured by [3H]dihydroalprenolol binding and cAMP production was similar in hypertensive and normotensive subjects.
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PMID:Adrenergic receptor function is different in male and female patients with essential hypertension. 23 16

Prostacyclin (PGI2) is known to cause vasorelaxation and inhibit platelet aggregation by receptor-mediated mechanisms. While cyclic (c) AMP is known to act as a second messenger for inhibition of platelet aggregation, vasorelaxation by hyperpolarization has been described only recently and may provide an explanation, in addition to stimulation of cAMP for the PGI2 mechanism of action on blood vessels. When PGI2 is infused into healthy volunteers it reduces blood pressure only at infusion rates that also cause significant side-effects, primarily, nausea, emesis, flushing, diaphoresis, and restlessness. In hypertensive patients blood-pressure responses are complex and are influenced to some extent by renin secretion. PGI2 stimulates renin secretion by a direct effect on the juxtaglomerular apparatus, and it also has an indirect effect by activating the sympathetic nervous system. Thus, it is useless as an antihypertensive agent even apart from its debilitating side-effects. Vascular PGI2 is synthesized endogenously by both the endothelial cells and the muscularis of arteries. While the endothelial cells undoubtedly synthesize large amounts of PGI2, the muscularis comprises a much larger tissue mass so that the overall synthesis is about equally distributed between the endothelial and muscle cells. In patients with pregnancy-induced hypertension and some patients with essential hypertension endogenous synthesis of PGI2 has been evaluated by measuring 2,3-dinor-6-keto-PGF1 alpha and has proved to be greatly reduced. Some drugs (thiazides, propranolol) have been shown to stimulate PGI2 synthesis, and inhibition of cyclooxygenase has been shown to reduce their antihypertensive effects. The effects of low- and high-dose aspirin on prostacyclin and thromboxane synthesis are discussed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Prostacyclin in hypertension]. 149 51

The interplays between calcium metabolic indices, retinal vascular status, plasma renin activity and blood pressure were examined in 67 patients with untreated essential hypertension. There was an inverse relationship between plasma ionized calcium and blood pressure (P = .002), whereas albumin-modified total serum calcium was directly related to blood pressure (P = .02). The plasma cyclic AMP level (P = .05) and the 24 h urinary excretion of cyclic AMP (P = .03) were also positively associated with blood pressure. Patients with vascular retinopathy had lower plasma ionized calcium concentrations (P = .01) and higher 24 h urinary cyclic AMP excretions (P = .05) than those without such changes, even when the differences in blood pressure, age, sex and body mass index were taken into account in analyses of covariance. Plasma renin activity did not interfere with the relationships between calcium metabolic indices and blood pressure, nor were there any associations between the renin status and the calcium metabolic indices. These findings suggest that a low concentration of plasma ionized calcium is an independent risk factor for vascular disease.
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PMID:Calcium metabolic indices, vascular retinopathy, and plasma renin activity in essential hypertension. 208 Oct 11

Prostacyclin (PGI2) is known to cause vasorelaxation and inhibit platelet aggregation by receptor-mediated mechanisms. While cyclic (c)AMP is known to act as a second messenger for platelet aggregation, vasorelaxation by hyperpolarization has been described only recently and may provide an explanation, in addition to stimulation of cAMP, for the PGI2 mechanism of action on blood vessels. When PGI2 is infused into healthy volunteers it reduces blood pressure only at infusion rates that also cause significant side effects, primarily nausea, emesis, flushing, diphoresis and restlessness. In hypertensive patients blood pressure responses are complex and are influenced to some extent by secretion. PGI2 stimulates renin secretion by a direct effect on the juxtaglomerular apparatus, and also has an indirect effect by activating the sympathetic nervous system. Thus it is useless as an antihypertensive agent even apart from its debilitating side effects. Vascular PGI2 is synthesized endogenously by both the endothelial cells and the muscularis of arteries. While the endothelial cells undoubtedly synthesize larger amounts of PGI2, the muscularis comprises a much larger tissue mass so that the overall synthesis is about equally distributed between the endothelial and muscle cells. In patients with pregnancy-induced hypertension and some patients with essential hypertension, endogenous synthesis of PGI2 has been evaluated by measuring 2,3-dinor-6-keto-PGF1 alpha and has proved to be defective. Some drugs (cicletanine, thiazides, propranolol) have been shown to stimulate PGI2 synthesis, and inhibition of cyclooxygenase has been shown to abolish their antihypertensive effects. Whether stimulation of PGI2 synthesis affects the antihypertensive efficacy of these drugs is not yet known.
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PMID:Prostacyclin in hypertension. 225 88

Various physiological changes of platelets and the vascular smooth muscle cell are intimately related. For this reason, in addition to the number of features in common between platelets and vascular smooth muscle and the increased risk for thromboembolic complication in essential hypertension, the platelet was used as an experimental model for the investigation of calcium-dependent functional anomalies associated with hypertension. It is demonstrated, by a sequential analysis of receptor and postreceptor events, that platelets in hypertension exhibit (a) a greater adenylate cyclase-activation and c-AMP-accumulation response to PGE1, (b) an enhanced epinephrine-induced phosphorylation response, and (c) an increased shape change sensitivity to serotonin and epinephrine. The anomalies in these calcium-dependent processes are linked to elevated free calcium concentrations in platelets from hypertensive subjects.
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PMID:Platelets and hypertension. 241 69

The properties of platelet alpha 2-adrenoceptors and of lymphocyte beta 2-adrenoceptors were determined in 40 male patients with established essential hypertension and compared with those in 40 male normotensives. The densities of platelet alpha 2-adrenoceptors (assessed by 3H-yohimbine binding) and of lymphocyte beta 2-adrenoceptors [determined by (+/-)-125iodocyanopindolol binding] were in patients with essential hypertension significantly higher than in controls; there were significant positive correlations between the mean arterial blood pressure of the subjects and alpha 2- and beta 2-adrenoceptor density, respectively. Concomitantly with receptor densities, functional responses to adrenergic stimulation were exaggerated in essential hypertension: in platelets, the aggregatory response to (-)-adrenaline (via alpha 2-adrenoceptor stimulation) was enhanced; in lymphocytes, the cyclic AMP response to (-)-isoprenaline (via beta 2-adrenoceptor stimulation) was elevated. It is concluded that the increased adrenoceptor density and responsiveness in circulating blood cells of patients with essential hypertension may reflect increased sympathetic activity, which might contribute to the elevation of blood pressure.
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PMID:Properties of alpha- and beta-adrenoceptors in circulating blood cells of patients with essential hypertension. 241 81

Essential hypertension is associated with various cell abnormalities, including alterations in the metabolism of intracellular messengers, such as cytosolic free Ca2+ and cyclic AMP or IP3. Intracellular pH is implicated in the regulation of number vital functions, including cell metabolism, division and response to various stimuli. We have measured cytosolic H+ concentration ([H+]i) in human platelets and investigated a possible relationship with free Ca2+ concentrations ([Ca2+]i) in hypertensive patients. [H+]i was determined with the pH sensitive fluorescent probe BCECF in platelets from 15 normotensive subjects and 15 patients with mild to moderate essential hypertension, free from medication, il any, for at least two weeks. Donor characteristics are indicated in the table. (table; see text) [H+] cytosolic from hypertensive patients was significantly lowered by 21 p. 100 compared to normotensive values (table). Cytosolic free Ca2+ concentrations, measured with the Ca2+ fluorescent probe Fura2, were significantly increased by 19 p. 100 in platelets from hypertensive patients when compared to those of normotensive donors. Taken all together, [H+]i and [Ca2+]i varied inversely (r = -0.421, p = 0.02) in these thirty donors and tends to be correlated in the essential hypertensive patients (r = 0.490, p = 0.06). This correlation remained significant at constant age systolic and diastolic blood pressures. The simultaneous rise in [H+]i and [Ca2+]i in platelets from essential hypertensive patients are compatible with their observed enhanced sensitivity to several aggregating agents. This alkalinisation, if present in the vascular smooth muscle cells, may also reflect facilitated cell proliferation and increased sensitivity to stimulating agents, two parameters implicated in the rise of arterial blood pressure.
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PMID:[Essential hypertension and platelet cytosolic concentrations of H(+) and Ca2(+)]. 251 Jun 44

Various abnormalities in platelet metabolism, including increased sensitivity to several aggregating agents, have been described in essential hypertension. Platelet response is controlled by Ca2+ and cyclic AMP-dependent mechanisms (stimulatory and inhibitory, respectively) which oppose one another. In the present study, the cyclic AMP contents of unstimulated platelets were measured by radio-immunoassay and observed to be lower in hypertensive than in normotensive subjects, either in the basal state or after prostaglandin E1 (PGE1) stimulation. In the presence of 7-bromo-1,5,dihydro-3,6-dimethylimidazo [2,1-b] quinazolin-2(3H)-one (Ro 15-2041), a specific inhibitor of phosphodiesterase, the increases in cyclic AMP content were similar in platelets from both groups, indicating that this enzyme was not responsible for the alterations in cyclic AMP metabolism observed in hypertension. Low external Ca2+ reduced basal and PGE1-stimulated cyclic AMP content in both normotensive and hypertensive groups but cyclic AMP levels remained lower in hypertensive patients than in normotensive subjects, indicating that Ca2+ influx is not responsible for this altered metabolism of cyclic AMP in hypertension. These data suggest that the reduced platelet cAMP content may participate in the hyperreactivity to various aggregating agents previously reported to accompany essential hypertension.
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PMID:Platelet cyclic AMP in essential hypertension. 255 May 42


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