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

The authors examined 74 women in III trimester (29-40 week), among them 44 women with hypertension induced by pregnancy (group examined) and 30 healthy women (control group). The blood serum of these women was studied for: creatinine, urea, uric acid, electrolytes K+ and Na+. Besides, the blood was studied for acid-base equilibrium (apparatus Corning type 128). The 24-hour urine of the two groups was studied for the concentrations of ions: 1) ammonium (NH4+), 2) hydrogen (H+) and 3) potassium and sodium (K+ and Na+). The authors also made the endogenic creatinine clearance (Ckr). The results were calculated statistically. The women with hypertension induced by pregnancy had in their blood serum an increase in the concentration of creatinine, urea and uric acid. As to the parameters of acid-base equilibrium, the authors found an increase in pCO2. Besides, the women with this kind of hypertension had: a decrease in the excretion of ions NH4+ and H+ in the urine, a decrease of Ckr with electrolytes K+ and Na+ being within the normal range.
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PMID:[Kidney function in women with pregnancy-induced hypertension]. 263 83

This experiment was carried out to elucidate how tumor microcirculation differs from that of normal tissues. Pressure-flow relationship was examined in normal rat tissues, uninvolved tissues in tumor-bearing rats, transplanted AH109A solid tumors, and primary tumors induced by 3-methylcholanthrene. Tumor blood flow was measured by the hydrogen clearance technique. The blood pressure was elevated by continuous iv infusion of angiotensin II. Elevation of blood pressure produced a several-fold increase in tumor blood flow without increasing blood flow in normal tissue and uninvolved tissue in tumor-bearing rats. The increase was selective to tumor tissues as long as the mean arterial blood pressure remained under about 150 mmHg. The lower the resting tumor blood flow, the greater the increase in the flow was at induced hypertension. There were no significant differences in the resting blood flow and in the rate of flow change at induced hypertension between the intramuscularly transplanted tumor, the intrahepatically transplanted tumor, and the sc transplanted tumor. These results indicate that the delivery of systemically administered anticancer drugs could be selectively enhanced in tumor tissues by induced hypertension.
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PMID:Functional characteristics of tumor vessels: selective increase in tumor blood flow. 264 66

Dietary sodium intake has long been considered important in the genesis and maintenance of hypertension. This view is predicated on the results of epidemiologic observations, experiments in animals, investigations at the cellular level, and the results from dietary intervention trials. In the past decade a considerable body of new evidence has been gathered. A comprehensive, world-wide epidemiologic investigation involving over 10,000 subjects found significant relationships between sodium excretion and blood pressure levels and between sodium excretion and the slope of increase in blood pressure with age. The relationships, however, are not as straight-forward as previously proposed. Investigations in animals and in human subjects emphasize the genetic nature of salt sensitivity of blood pressure. A putative genetic marker has been suggested in human studies. At the cellular level, increases in sodium-lithium countertransport, sodium-hydrogen exchange, and cytosolic calcium level have been identified. Cytosolic calcium level was found to increase in lymphocytes in response to a high-salt diet in salt-sensitive individuals with hypertension, yet the identification of a circulating inhibitor of sodium-potassium--dependent adenosine triphosphatase remains elusive. Dietary intervention trials of salt restriction in patients with hypertension are generally disappointing. Active research is elucidating the role of sodium intake and hypertension at all levels. The data to date, however, still do not allow sweeping conclusions or generalizations.
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PMID:Salt and hypertension: recent advances and perspectives. 267 Dec 14

We looked at the relation between systemic arterial blood pressure and recovery from spinal cord injury by inducing both hypertension and hypotension in 25 rats randomly allocated to five equal groups. The rats received no injury, a mild (2.3-g), or a severe (53.0-g) spinal cord injury lasting 1 minute. We used the hydrogen clearance technique to measure spinal cord blood flow at the injury site (T1) and at an adjacent site (C6). Mean systemic arterial blood pressure was either increased with adrenaline or decreased by phlebotomy in 20-mm-Hg intervals except for the severe-injury group, in which the posttraumatic pressure could only be increased with adrenaline. Spinal cord blood flow remained constant in the no-injury group between 81 and 180 mm Hg. After a mild injury, induced moderate hypertension (121-140 mm Hg) improved spinal cord blood flow significantly, whereas hypotension decreased it in a linear fashion. Severe injury caused a marked decrease in spinal cord blood flow and mean systemic arterial blood pressure. Even extreme hypertension (161-180 mm Hg) induced by adrenaline did not significantly increase spinal cord blood flow at T1 but caused hyperemia at C6 due to loss of autoregulation. In conclusion, normotension should be attempted, irrespective of the severity of spinal cord injury. Induced hypertension after severe spinal cord injury was not beneficial in improving spinal cord blood flow at the injury site while potentially increasing hemorrhage and edema.
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PMID:Spinal cord blood flow and systemic blood pressure after experimental spinal cord injury in rats. 292 76

Angiotensin-converting enzyme inhibitors promise to make important therapeutic contributions to the control of hypertension and congestive heart failure. The nonapeptide teprotide was the first of these inhibitors to be tested clinically. It was followed by orally active inhibitors, captopril in 1977 and enalapril in 1980. The latter is representative of a new design for the inhibition of metallopeptidases and is the subject of this review. The best of the N-carboxyalkyldipeptide inhibitors inhibits angiotensin-converting enzyme with a Ki of 7.6 X 10(-11) M. This compound is the most potent competitive inhibitor of a metallopeptidase yet to have been reported. The basis of this high potency is beginning to be understood and in part is considered to involve precisely arranged multiple interactions within the enzyme active site. X-ray crystallography of a thermolysin-inhibitor complex has been achieved. Assuming that similar interactions within the active site of angiotensin-converting enzyme are mechanistically probable, the authors hypothesize the binding of enalaprilat to converting enzyme as shown in Figure 24. Such interactions are consistent with kinetic studies (Section V) with the understanding that binding to the enzyme is not sensitive to the inhibitor's state of NH protonation. The reason for this surprising conclusion has not been established. Perhaps counterbalancing factors are involved in the energetics of binding or there may be compensating adjustments made in the enzyme which permit NH protonated and nonprotonated inhibitor to bind equally well. Figure 24 also summarizes present understanding of the conformation of enalaprilat when bound to angiotensin-converting enzyme. From studies on conformationally defined analogs of enalaprilat, it seems likely that the Ala-Pro segment of enalaprilat binds in a conformation that is close to a minimum energy conformer. This situation no doubt contributes to the potency of enalaprilat, since little binding energy would be needed to induce conformational changes in this part-structure of enalaprilat when it is bound to the enzyme. The phenethyl group of enalaprilat is believed to be near the alpha-hydrogen of the L-Ala residue in the enzyme-inhibitor complex. However, the synthesis of conformationally restricted analogs to establish this point has not yet been reached. The N-carboxyalkylpeptide design was developed from Wolfenden's collected product inhibitors of carboxypeptidase-A. Whether or not N-carboxyalkyldipeptides should be classified as collected product or transition state inhibitors is unclear.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The design and properties of N-carboxyalkyldipeptide inhibitors of angiotensin-converting enzyme. 299 4

Acute, severe increases in arterial blood pressure cause sustained cerebral arteriolar dilation, abnormal reactivity to carbon dioxide and to changes in blood pressure, abolition of endothelium-dependent dilation from acetylcholine, discrete morphological lesions of the endothelium and vascular smooth muscle, and breakdown of the blood-brain barrier to plasma proteins. The dilation, abnormal reactivity, and morphological abnormalities are inhibited by pretreatment with cyclooxygenase inhibitors or with free radical scavengers. Superoxide dismutase-inhibitable reduction of nitroblue tetrazolium applied to the brain surface was detectable both during hypertension and one hour after hypertension subsided. Nitroblue tetrazolium reduction is also reduced by inhibitors of the anion channel. The abnormalities seen after hypertension are reproduced by topical application of arachidonate. The results are consistent with the view that acute hypertension induces generation of superoxide anion radical in association with accelerated arachidonate metabolism via cyclooxygenase. This radical enters cerebral extracellular space via the anion channel and gives rise to hydrogen peroxide and hydroxyl radical. All three radicals are capable of causing vasodilation by relaxation of cerebral vascular smooth muscle. The hydroxyl radical is the most likely candidate for vascular wall damage. The significance of this mechanism in chronic experimental hypertension or its relevance to human disease is not known.
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PMID:George E. Brown memorial lecture. Oxygen radicals in cerebral vascular injury. 299 3

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

alpha 2-Adrenoceptors were first described pharmacologically ten years ago. Within three years their capacity to inhibit adenylate cyclase had been demonstrated in many tissues. They were demonstrated biochemically in the kidneys in 1981 even before any renal physiological effects of their activation were known. They predominate numerically over alpha 1-adrenoceptors in renal membranes and their density is increased in genetic forms of rat hypertension. alpha 1-Adrenoceptors normally mediate the vasoconstriction and sodium- and water-retaining effects of sympathetic neuronally released norepinephrine. Norepinephrine or epinephrine must be infused to activate alpha 2-adrenoceptors, suggesting that renal alpha 2-adrenoceptors are extrajunctional, whereas alpha 1-adrenoceptors are postjunctional. When alpha 1-adrenoceptors are chronically blocked, renal alpha 2-adrenoceptor density increases and they assume a location at postjunctional sites, the otherwise exclusive domain of alpha 1-adrenoceptors. Results from microdissection studies have established that alpha 2-adrenoceptors are present on most segments of the nephron and that their activation can suppress adenosine 3,'5'-cyclic monophosphate (cAMP) accumulation induced by most renal hormones. However, failure of alpha 2-adrenoceptor activation to suppress cAMP accumulation in some tubular segments induced by certain hormones suggests compartmentalization of adenylate cyclase regulation that is hormone-function specific. In view of the potent inhibitory effects of alpha 2-adrenoceptor stimulation on hormone activated cAMP accumulation in several discrete areas of the nephron, we suggest that alpha 2-adrenoceptors fulfill important regulatory role(s) in renal function. To date, alpha 2-adrenoceptor activation has been shown to reverse vasopressin-induced sodium and water retention, and arachidonic acid- and furosemide-induced cAMP, sodium, and water excretion in the isolated perfused kidney. Thus the effects are qualitatively and quantitatively dependent in these studies on the hormone being infused and are therefore hormone-function specific. Physiological effects of alpha 2-adrenoceptor activation of thyrocalcitonin and on parathyroid hormone-induced effects have not been studied. alpha 2-Adrenoceptor activation can inhibit renin release in some model systems and can activate a sodium-hydrogen antiporter system in proximal tubules. The physiological roles of these actions are unknown.
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PMID:Renal alpha 2-adrenoceptors and the adenylate cyclase-cAMP system: biochemical and physiological interactions. 302 68

Experiments were designed to investigate the importance of vascular endothelium in the vasomotor response to increases in flow as observed in conduit arteries (flow-dependent dilation). The diameter changes of femoral arteries (sonomicrometry) in response to increases in flow before and after endothelial damage procedures were studied in 23 dogs anesthetized with sodium pentobarbital. The functional integrity of the endothelial cells underneath the diameter sensors was tested by intra-arterial acetylcholine (local acetylcholine dilation) applied proximally to the sensors while a constant flow was maintained. Unilateral augmentation of femoral arterial flow (4.6 +/- 1.9-fold) induced by peripheral vasodilation or by arteriovenous shunt, elicited dilation (increase in diameter, 116 +/- 91 microns) in 18 of 23 dogs, whereas the diameter of the contralateral control artery was not affected. Mechanical removal of the endothelial cells by means of a balloon catheter abolished both the flow-dependent dilation and the local acetylcholine dilation, whereas the vasomotor responses to norepinephrine and nitroglycerin were not affected. Brief perfusions (1 minute) of the arteries with cell-free hydrogen peroxide solution (90 mM) also abolished the flow-dependent dilation and attenuated the local acetylcholine dilation (by 27 +/- 19%; p less than 0.02), while the responses to norepinephrine and nitroglycerin were not altered. These results suggest that endothelial cells act as mediators of flow-dependent dilation.
Hypertension 1986 Jan
PMID:Crucial role of endothelium in the vasodilator response to increased flow in vivo. 308 Mar 70

The circulatory effects of oleanoic acid sodium hydrogen succinate (OSS), an analogue of the anti-ulcer drug, carbenoxolone, were investigated. As carbenoxolone produces such adverse effects as sodium retention and a subsequent elevation of the arterial blood pressure in man, the present study was aimed at determining whether OSS is similar or different from it in this respect. Carbenoxolone, (43,3 mg/kg po) and OSS (66,6 mg/kg po) were given to rats twice daily for 4 weeks. The systolic blood pressure was elevated already after the first week of treatment. The hypertension was accompanied by bradycardia, which increased with the time of treatment. In the blood an increase in the creatinine level, a decrease in the urea level, and a slight elevation in sodium concentration were found after the treatment, while the potassium concentration during the whole treatment period (4 weeks) remained unchanged. Although the principal aldosterone-like effects of carbenoxolone were attributed to the oxygen presence in position 11 of the glycyrrhetinic acid ring, [8], the absence of an oxygen at that position in OSS did not cause the loss of the adverse circulatory effect.
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PMID:Cardiovascular action of a new carbenoxolone derivative. 324 64


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