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

In order to find out whether adrenoceptor changes in essential hypertension might be genetically determined, we measured platelet alpha 2- and lymphocyte beta 2-adrenoceptor density in 48 normotensive children with normotensive parents, and 41 normotensive children who had one essential hypertensive parent and thus should have had a genetic predisposition for the development of hypertension. The groups did not differ with regard to blood pressure and heart rate, age, body weight and height, plasma renin activity and catecholamines, and serum electrolytes and creatinine. Lymphocyte beta 2-adrenoceptor density (assessed by 125I-iodocyanopindolol binding) and responsiveness (assessed as 10 mumol/l isoprenaline-induced cyclic AMP increases) did not differ between the groups. Platelet alpha 2-adrenoceptor density (assessed by 3H-yohimbine binding) was significantly higher in children with one essential hypertensive parent. We conclude that platelet alpha 2- but not lymphocyte beta 2-adrenoceptor changes in essential hypertension are genetically determined.
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PMID:Are alpha- and beta-adrenoceptor changes in patients with essential hypertension genetically determined? 285 61

Beta-adrenoceptor blockade (beta-blocker) has recently been introduced for use in treating hypertension of pregnancy. The aim of this investigation is to determine the effects of beta-blocker (alprenolol and labetalol) on parturition and on the fetal cardiovascular and metabolic system in normotensive pregnant rats. The continuous administration of alprenolol to pregnant Wistar rats revealed the following: a small placenta intrauterine growth retardation delayed parturition intrauterine death (21.8%) morbidity (30.3%) and, hypoglycemia of neonates. In the cases which received the administration of both labetalol and alprenolol, the growth of fetuses was retarded. However, there was twice as much growth retardation of the fetuses treated with alprenolol. No other abnormalities were observed. The administration of alprenolol in pregnant rat uteri (in vitro) resulted in stimulation of myometrial contractility (oxytocic reaction) and lowered the c-AMP levels in the bath medium. However, when labetalol was administered, uterine activity was reduced in a dose-dependent manner (tocolytic reaction) with a concurrent rise in c-AMP levels in the bath medium. The effect of alprenolol on rat uterine blood flow using the thermocouple method resulted in a decrease of 18-30 percent but with labetalol there was only a slight decrease (0-5%).
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PMID:[Effects of beta-adrenoceptor blockade on parturition and fetal cardiovascular and metabolic system]. 286 Jan 90

The discovery that monoamine nerves end on the central microvessels of the choroid plexus, pia-arachnoid and parenchyma has prompted an intense investigation as to their physiological and neuropathological roles. The source of the monoamine fibers to the pial vessels and choroid plexus was shown to be the superior cervical ganglion. Ganglionic stimulation causes vasoconstriction or vasodilation of pial vessels, an event depending upon the functional ratio of alpha to beta adrenergic receptors. Moreover, stimulation of the superior cervical ganglion evokes an inhibition of cerebrospinal fluid formation in choroid plexus. The locus coeruleus is the site of adrenergic nerve supply to the parenchymal capillaries and stimulation of this nucleus increases capillary permeability to small molecules and water. Neurotransmitter receptors (adrenergic, histamine, adenosine, dopamine, prostacyclin, prostaglandins and specific amino acids or neuropeptides) have been identified on microvessels and in many instances these transmitter actions are coupled to cyclic AMP synthesis. Moreover, cyclic AMP has been shown to increase the rate of capillary endothelial pinocytosis and produce brain edema. In small vessels containing smooth muscle cells cyclic AMP production improves cerebral blood flow via an initiation of vasodilatory processes. The presence of receptors for serotonin and acetylcholine have likewise been demonstrated to occur on cerebral microvessels. Limited information is available as to the receptor coupled actions of these two transmitters, but cholinergic mechanisms may act to restrict catecholamine-induced formation of cyclic AMP. Altered sensitivity of microvessels to neurotransmitters has been demonstrated following conditions of stroke, hypertension, aging, diabetes and X-irradiation.
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PMID:Neurochemical coupled actions of transmitters in the microvasculature of the brain. 287 36

The effects of three different types of beta-adrenoceptor blocking agents on platelet aggregation and on platelet and plasma cyclic AMP content have been studied in 14 patients with mild hypertension given each drug in turn for two weeks. The drugs were a non-selective blocking agent with high intrinsic sympathomimetic activity, pindolol, the nonspecific blocking agent propranolol, and the beta 1-selective metoprolol. The threshold values of ADP and adrenaline for irreversible platelet aggregation were significantly higher for pindolol and metoprolol than for propranolol. The cyclic AMP content of platelets was higher during pindolol and metoprolol than during propranolol treatment. Pindolol produced a substantial increase in plasma cyclic AMP relative to the other two drugs. Thus, platelet aggregation and cyclic AMP formation are influenced by beta-adrenoceptor blockade in proportion to intrinsic sympathomimetic activity and affinity for different beta-adrenoceptor subtypes.
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PMID:Effects of three beta-blockers with different pharmacodynamic properties on platelet aggregation and platelet and plasma cyclic AMP. 290 89

A total of 112 patients with borderline arterial hypertension and essential hypertension of the labile and stable forms were examined. The plasma levels of cyclic AMP and cyclic GMP as well as the renin activity of the blood were determined in all those studied both at rest and following insulin administration. The findings obtained point to a certain role of cyclic nucleotides in the development and stabilization of arterial hypertension.
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PMID:[Reaction of cyclic plasma nucleotides of healthy subjects and essential hypertension patients to insulin stimulation]. 298 50

Vascular cyclic AMP alterations were studied during the initiation of vascular hypertrophy and hyperplasia in spontaneously hypertensive rats (SHR). The onset of hypertension at 6 weeks of age coexisted with a three-fold elevation in the aortic content and concentration of cyclic AMP, whereas aortic DNA and protein contents were identical to those of WKY controls. A similar cyclic AMP elevation was present in 12-week-old SHR when vascular hypertrophy and hyperplasia were already established. These experiments suggest the participation of cyclic AMP in the process of hypertensive vascular growth.
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PMID:Elevated arterial cyclic AMP levels during the development of spontaneous hypertension in rats. 299 2

The widespread use of beta-adrenoceptor antagonists against hypertension, angina pectoris and migraine or as a preventive treatment after myocardial infarction has encouraged us to investigate the effects of these drugs on platelet function. The aim of this study was to examine whether beta-blocking drugs interfere with platelet beta- adrenoceptors and whether this dependency is related to their selectivity for beta-adrenoceptor subtypes. Beta-adrenoceptor stimulation of human platelets with isoprenaline increased cyclic AMP (cAMP), which is known to inhibit platelet aggregation. Furthermore, our studies showed that cAMP formation in vitro was stimulated by non-selective and beta 2-selective agonists, but not by the predominant beta 1-agonist prenalterol. Isoprenaline- stimulated cAMP formation was blocked by the non- selective beta-adrenoceptor antagonists propranolol, timolol, and alprenolol, while the beta 1-selective antagonists atenolol and metoprolol had no influence on an isoprenaline-induced cAMP formation. Receptor binding studies using (3H)-dihydroalprenolol revealed an IC50 value for propranolol of 85 nM, while metoprolol only displaced the bound (3H)-dihydroalprenolol at far higher concentrations (IC50, 20 microM). We conclude that the human platelet beta-adrenoceptors are mainly of the beta 2- subtype and that beta-adrenoceptor antagonists, especially the non-selective antagonists interfere with platelet function assessed as platelet cAMP formation.
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PMID:Characterization of human platelet beta-adrenoceptors. 300 61

The susceptibility to cerebral ischemia was studied in stroke-resistant spontaneously hypertensive rats (SHRSR) treated by a long-term antihypertensive treatment, and compared with untreated SHRSR and Wistar rats (WR). Male SHRSR, aged 8 weeks, were divided into two groups and a long-term antihypertensive treatment for 4-6 weeks was started on one group (treated SHRSR: T-SHR) while the other group was left untreated as control (untreated SHRSR: U-SHR). The changes of blood pressure were checked on these rats. The prior treatment of hypertension was achieved by administration of hydroflumethiazide (120 mg/kg/day) and captopril (15-30 mg/kg/day) orally for 4-6 weeks by mixing in drinking water. All the experiments were performed at the age of 12-16 weeks and WR of similar age served as normotensive untreated control. Cerebral ischemia was induced by bilateral common carotid artery ligation (BLCL) and blood pressure was always checked before BLCL. The survival ratio was observed from 1 hour to 24 hours after BLCL. The regional cerebral blood flow (rCBF) were measured before and 4 hours after BLCL periodically. The brain energy metabolites were measured 4 hours after BLCL. rCBF were measured at the thalamus by the hydrogen clearance method. ATP concentrations were determined by luciferine-luciferase method, c-AMP was measured by RIA and lactate by enzymatic method. The brain water content was measured by freeze-dry method.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of long-term prior antihypertensive treatment on cerebral ischemia induced by bilateral common carotid artery ligation in SHRSR]. 300 93

In a prospective study of 21 normal human kidney donors, increases in blood pressure were found in seven of 12 males and in three of nine females within the first year after uninephrectomy. Donors with blood pressure increases were characterized by greater weight and body mass indexes. In addition, urinary phosphate excretion was positively correlated (r = 0.73, p less than 0.001) and tubular reabsorption of phosphate negatively correlated (r = -0.61, p less than 0.01) with blood pressure at the follow-up periods in which increases were observed. All donors experienced an increase in parathyroid hormone levels and urinary cyclic AMP excretion. These changes were accompanied by decreases in urinary calcium and serum phosphate values. Thus, the increase in blood pressure took place in a milieu similar to that of "normocalcemic" hyperparathyroidism. The correlation of phosphate excretion and blood pressure in normal donors suggests an important role for phosphate metabolism in the genesis of hypertension associated with loss of renal mass.
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PMID:Divalent ion handling in human kidney donors with increased blood pressure after uninephrectomy. 301 74

By use of tritiated arginine-8-vasopressin (AVP), vasopressin specific binding sites were detected on Sprague-Dawley rat urinary bladder and spleen. In both tissues, one class of high-affinity binding sites was characterized with an equilibrium dissociation constant of 1.61 +/- 0.22 and 1.91 +/- 0.16 nM and a maximal binding capacity of 155 +/- 5 and 110 +/- 11 fmol/mg of protein, for bladder and spleen, respectively. In both tissues, several experimental arguments suggest that these receptors belong to the V1-vascular type: Highly significant correlations were found between the relative agonistic vasopressor activities of eight AVP agonists and their relative abilities to inhibit [3H]AVP binding to the receptors, whereas no such relationship existed when antidiuretic activities were considered. The same profile was also observed with the antagonistic activities of five AVP antagonists. Moreover, AVP (10(-12)-10(-5) M) did not modify the basal cyclic AMP production in either tissue. As cyclic AMP is known to respond to V2 stimulation, the data suggest that the receptors measured are the V1 type. In Dahl rats the receptor characteristics were modulated by salt diet. More interestingly, the number of spleen vasopressin binding sites was always lower in Dahl salt-resistant animals than in the Dahl salt-sensitive animals receiving either a sodium deficient or a 1% NaCl or an 8% NaCl-containing diet. The exploration of vasopressin receptors regulation should facilitate the comprehension of the role played by AVP in different models of experimental hypertension.
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PMID:Characterization of vasopressin receptors of rat urinary bladder and spleen. 301 3


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