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

Interrelations among blood pressure, circulatory volume, plasma renin activity (PRA) and urinary catecholamine excretion rates were studied in normal subjects and in patients with benign essential hypertension. Mean plasma or blood volumes related to lean body mass, products of blood volume and the logarithm of PRA, and catecholamine excretion rates did not differ significantly between normal and hypertensive subjects. In both normal subjects and hypertensive patients, blood pressure levels correlated positively with the noradrenaline excretion rate (r = 0.40 and 0.36, respectively; p less than 0.025) but not with adrenaline excretion, circulatory volume or the volume-renin product. The logarithm of PRA correlated inversely with mean blood pressure in normal subjects (r = 0.40; p less than 0.001) but not in hypertensive patients; however, there was no convincing evidence for an inappropriate blood pressure-PRA relationship as a prominent feature in the hypertensive patients. PRA did not correlate with blood volume. Patients with low PRA relative to sodium excretion (21 per cent of hypertensive population) were consistently normovolemic, but they tended to be older and excreted less (p less than 0.025) adrenaline than patients with normal or high PRA. The patient subgroup with high PRA relative to sodium excretion (11 per cent of population) was hypovolemic (p less than 0.02); despite this, urinary sodium output was high (172 +/- 64 meq/24 hours). These data reveal no evidence for major roles of PRA, circulatory volume and free peripheral catecholamines in the maintenance of benign essential hypertension. Essential hypertension with low PRA is usually not a hypervolemic state, but it may reflect diminished adrenergic activity, factors associated with aging and effects of a high systemic pressure. High PRA in benign essential hypertension may be at least partly a consequence of hypovolemia resulting from high blood pressure-induced sodium diuresis.
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PMID:Interrelations among blood pressure, blood volume, plasma renin activity and urinary catecholamines in benign essential hypertension. 83

Properties of the longitudinal smooth muscle of portal veins from normotensive Wistar rats, adult (NCR) and young (NCRy); spontaneously hypertensive Okamoto rats, adult (SHR) and young (SHRy); and adult Wistar rats with renal hypertension (RHR) were studied in vitro and histologically. Some aortic strips from SHR and SHRy were compared with controls. In response to noradrenaline (NA) and acetylcholine (ACh) greater maximum force was developed by veins from all hypertensive groups than by those from control rats. Cross-sectional area of the longitudinal muscle of veins from SHR but nor SHRy nor RHR was greater than control. Maximum stress in response to agonists was greater in both SHR and RHR than NCR. ED50-values for NA and ACh were lower in portal veins from SHR than NCR but not from RHR nor SHRy compared to controls. Denervation did not abolish any of the differences between SHR and NCR. Aortic strips from SHR developed less maximum force to NA and ED50 was greater than those from NCR, i.e. opposite to the findings in portal veins. Low levels of external Ca2+ reveal altered calcium handling in veins from SHR compared to controls. It is concluded that portal veins from hypertensive rats are functionally different from those of normotensive rats and differ in SHR compared to RHR. It is suggested that the altered functional properties of portal vein, but not of aorta, in several respects resemble those of arterial resistance vessels. The implications of these findings are discussed in terms of mechanisms of hypertension in these animal models.
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PMID:Contractility, muscle mass and agonist sensitivity of isolated portal veins from normo- and hypertensive rats. 85 13

1. Plasma noradrenaline concentrations and dopamine beta-hydroxylase activity have been measured at various stages in the development of hypertension in the one-kidney Goldblatt rat (unilateral renal arterial constriction and contralateral nephrectomy). 2. Although plasma noradrenaline concentrations were significantly elevated from control values at 7, 14 and 28 days, plasma dopamine beta-hydroxylase activity was not significantly different from control values except at 24 h. 3. These findings suggest that peripheral sympathetic activity is increased in the one-kidney Goldblatt model of experimental hypertension but that plasma dopamine beta-hydroxylase activity is poor index of this increase. 4. Both the rise in blood pressure and the rise in plasma noradrenaline concentrations were prevented by pretreatment with intracisternal 6-hydroxydopamine, suggesting that the increased sympathetic activity is at least in part centrally mediated.
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PMID:Plasma noradrenaline concentrations in experimental renovascular hypertension in the rat. 86 41

A male aged 47 years with gross autonomic insufficiency as part of the Shy-Drager syndrome is described. He did not sweat normally when warmed, and his circulatory responses to mental arithmetic, the Valsalva manoeuvre, and head-up tilt were abnormal indicating severe sympathetic failure. During head-up tilt there was a rise in plasma renin activity and plasma aldosterone. It is argued that plasma renin activity is not dependent on sympathetic nervous activity and may be mediated by renal baroreceptors. These rises may help sustain the blood pressure in such patients during repeated head-up tilts. Infusions of L-noradrenaline and angiotension produced greater hypertension, and injections of isoprenaline greater hypotension than in controls. Although it is difficult to exclude the possibility that one factor in this may be hypersensitivity of receptors in blood vessel walls, the principal factor is likely to be the absence of those baroreflexes of which the efferent pathways are in the sympathetic nervous system.
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PMID:Postural changes in plasma renin activity and responses to vasoactive drugs in a case of Shy-Drager syndrome. 86 77

Catecholamines and catecholamine-synthesizing enzymes have been studied quantitatively in specific brain areas of spontaneously (genetically) hypertensive rats by means of a combination of sensitive enzymatic-isotopic methods and a microdissecting technique. Changes in catecholamine metabolism were found to be localized to regions of the brain implicated in the regulation of blood pressure. Noradrenaline levels were decreased in specific nuclei of the anterior hypothalamus and in the nucleus interstitialis striae terminalis ventralis. The activity of the adrenaline-forming enzyme, phenyl-ethanolamine-N-methyl transferase, was increased in the A1 and A2 areas of the brain stem. These results implicate catecholamine-forming neurons in the hypothalamus and brain stem in the development of spontaneous hypertension in rats.
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PMID:Biochemical and morphologic study of catecholamine metabolism in spontaneously hypertensive rats. 86 35

5-hydroxydopamine, unspecific centrally acting false neurotransmitter. Acta Physiol. Pol., 1977, 28 (1): 13-22. 3,4,5-trihydroxyphenetylamine-5-hydroxydopamine (5-OHDA) injected intracerebro-ventricularly decreases the level of noradrenaline, 5-hydroxytryptamine and 5-hydroxyindoleacetic acid in different parts of the rat brain. It does not affect acetylcholine level. 5-OHDA causes dose-dependent hypothermia, transient hypertension and depression of locomotor and exploratory activity in rats. This behavioral phenomena are reversed by central chemical sympathectomy elicited by 6-hydroxydopamine. It is concluded that 5-OHDA is an unspecific centrally acting false transmitter.
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PMID:5-hydroxydopamine, unspecific centrally acting false neurotransmitter. 86 21

Hypertension in spontaneously hypertensive rats (SHR) develops initially without any obvious organic lesions, and mainly with hemodynamic alteration due to increased peripheral vascular resistance. It is then followed later by various cardiovascular complications such as stroke. These facts indicate that this spontaneous hypertension is very similar to essential hypertension in man. Studies on the pathogenic mechanisms of spontaneous hypertension up to the present have revealed the following points. (1) This hypertension is genetically transmitted to the offspring in an additive mode by a relatively small number of major genes; (2) Environmental factors such as stress and salt-loading accelerate the hypertension; (3) Parabiosis between SHR and normotensive rats offered no positive evidence indicating the involvement of any strong humoral factors; (4) Assays on adrenal and thyroid hormones have suggested that this hypertension is not a simple endocrine hypertension; (5) The destruction of the central nervous system or sympathectomy on blood pressure or peripheral vascular resistance, as well as the recording of spontaneous sympathetic discharge, etc. have indicated the positive involvement of the autonomic nervous system in the development of this hypertension; (6) Changes in the enzyme activities of the central nervous system and in the central responses to various candidates of central neurotransmitters suggested that 'noradrenergic inhibitory mechanisms for blood pressure regulation in the brainstem' (Yamori, Lovenberg and Sjoerdsma, 1970) might be insufficient and result in the initial enhancement of peripheral vasomotor tone causing labile hypertension; (7) Noradrenalin turnover study of the heart and hindlimb perfusion experiments indicated that the neural factor was mainly involved in the development or the early stage of hypertension; this finding was further supported by the increased noradrenalin level or dopamine-beta-hydroxylase activity in the blood; (8) Histometrical studies indicated that the structural component of the peripheral vascular resistance stabilized the hypertension; (9) The initial neurogenic factors and successive involvement of nonneurogenic factors are relayed by the acceleration of protein metabolism of the vascular wall ('adaptive metabolic change', Yamori, 1974). This acceleration is commonly detected by amino acid incorporation study in both spontaneous and other experimental hypertension; (10) Increased lysine incorporation into the noncollagenous protein of the mesenteric arteries detected in the prehypertensive SHR was experimentally confirmed to be influenced by neural innervation. This confirmation indicated the importance of such a trophic effect of the nervous system on the structural alteration of blood vessels in the development of hypertension (neurovascular linkage, Yamori, 1975)...
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PMID:Pathogenesis of spontaneous hypertension as a model for essential hypertension. 87 Jul 22

For continuously measuring the circumference of the aorta in conscious rats for up to 20 days, a new electrolytic strain gauge of high sensitivity and stability was constructed of silicone tubing filled with copper nitrate. The mean systolic and diastolic circumferences measured in 11 nonanesthetized undisturbed rats were 6.557 +/- 0.128 mm and 6.533 +/- 0.128 mm, respectively--the pulse pressure (51 mm Hg) producing an increase of 0.024 mm in aortic size (0.37% increase of the diastolic circumference). The calculated dynamic elastic modulus was 13,908 dynes/cm2. Infusions of blood, angiotensin, and noradrenaline to increase mean aortic pressure acutely by 50 mm Hg caused aortic circumference to increase by 0.59, 0.58, and 0.53%, respectively. Seven rats were subjected to acute hypertension produced by subdiaphragmatic aortic constriction after recording the control measurements. Over the period of study (6 hours) after aortic constriction, mean aortic blood pressure was increased 50 mm Hg from the control of 101 mm Hg. A mean maximal increase of 6% in aortic circumference was seen at 3 hours and a mean minimum of 0.9% at 4 hours, with an average increase of 3% for the entire 6-hour period. These changes in aortic circumference coincide with an upward displacement of about 30% in the range of activation of the aortic baroreceptors.
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PMID:Continuous measurement of aortic caliber in conscious rats. Effect of acute hypertension. 87 66

The resistance of vessels in the hind limbs was determined under controlled perfusion in rats adapted to hypoxia at 2100 m altitude and in control animals at 200 m above the sea level. It was found that 15 days after the onset of adaptation the resistance of the resistive vessels decreases, after 30 days the degree of this decrease of resistance grows and it becomes statistically significant. The decrease of resistance in the resistive vessels of adapted animals persists after denervation of the extremity and depends on the reduction of the myogenic component of the vascular tonicity. This reduction of the myogenic component of the tonicity is accompanied by a reduction of the pressor reactions to asphyxia and addition of noradrenaline to the perfusate. The obtained data indicate that preliminary adaptation decelerates the development of experimentally induced hypertension.
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PMID:[Effect of adaptation to altitude hypoxia on vascular resistance]. 88 59

The relationship between the severity of hypertensive disease and sodium excretion and sympathetic activity has been studied in normotensive (n = 19) and hypertensive (n = 19) men of the same derived from screening a total population. Sympathetic activity was determined from noradrenaline excretion and the severity of hypertension was assessed by measuring resting diastolic BP, left ventricular hypertrophy on orthogonal ECG and the glomerular filtration rate. In the hypertensive group the resting BP correlated well both with signs of left ventricular hypertrophy, i.e. with the degree of severity of the hypertensive disease. Up to the level of 90 mm Hg resting diastolic BP, sodium excretion rose in agreement with theory of pressure diuresis. Above 90 mm Hg, however, both sodium and noradrenaline excretion fell with increasing BP. This indicated that in more advanced hypertension the sodium balance overrides the sympathetic activity in the long-term relation of BP. In another series of 49-year-old-men noradrenaline excretion fell with increasing renal vascular resistance indicating that the increase in the latter variable could not be explained by increased sympathetic tone. On the basis of the results a hypothesis on the sequence of events leading to development of hypertension, is presented.
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PMID:Sodium excretion and sympathetic activity in relation to severity of hypertension. 89 Dec 9


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