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

Experiments were conducted on 119 male and female mongrel/albino rats and on 5 male rabbits to study the mechanisms of the in vivo effect of the inhibitors of the biosynthesis of prostaglandins, acetylsalicylic acid, and indometacin, taking into account the previously obtained data on the fact that these inhibitors elevate mean arterial pressure and increase vasopressor sensitivity to adrenalin and noradrenaline in experimental animals. It was found that these inhibitors of prostaglandin biosynthesis promote the development of "salt hypertension" in rats against the background of a noticeable increase in vasopressor sensitivity to catecholamines. Intravenous administration to rabbits of angiotensin-11 in pressor doses causes an increase in the content of group E prostaglandins in the blood plasma of rabbits and a decrease in the renin activity ("feedback" effect). The data obtained have confirmed the assumption that prostaglandins take part in the arterial pressure control and suggested that in exhaustion or hereditary deficiency of the function of the prostaglandin production system the vessels may escape the depressor control, in this case the sensitivity to pressor factors increase and stable arterial hypertension develops.
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PMID:[Role of prostaglandins in blood pressure regulation]. 59 3

Previous work has shown that parathyroidectomy protected Sprague-Dawley rats against mineralocorticoid hypertension. 2 In order to explain this protection, we studied vascular reactivity to noradrenaline and angiotensin II in several groups of rats with and without their parathyroid and thyroid glands. Work was performed in vagotomized, anaesthetized rats after ganglionic blockade with pentolinium, and atropine sulphate. 3 The reactivity to noradrenaline was significantly lower in parathyroidectomized rats, especially at the beginning of mineralocorticoid treatment. 4 Autotransplantation of parathyroid glands in thyroparathyroidectomized rats re-established normal cardiovascular reactivity and development of hypertension. 5 Cardiovascular reactivity to angiotensin II was not affected in parathyroidectomized rats and was lowered in thyroparathyroidectomized thyroxine-treated rats.
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PMID:Effect of parathyroidectomy on cardiovascular reactivity in rats with mineralocorticoid-induced hypertension. 62 36

Catecholamines and catecholamine-synthesizing enzymes have been examined in specific brain areas during the development of spontaneously (genetic) hypertensive (SH) rats. Changes in catecholamine metabolism were localized to regions of the brain implicated in the regulation of blood pressure. Norepinephrine levels and dopamine-beta-hydroxylase (DBH) activities were decreased in specific nuclei of the hypothalamus and in the nucleus interstitialis striae terminalis ventralis, in both young and adult rats. The decrease in the formation of norepinephrine can result in a reduced activation of central alpha-adrenergic receptors which may be related causally to the onset of hypertension. The activity of the epinephrine-forming enzyme, phenylethanolamine-N-methyltransferase (PNMT), was increased in the A1 and A2 areas of the brainstem in young SH rats, but it was normal in adult hypertensive animals. These results implicate adrenergic neurons in the brainstem and noradrenergic neurons in the hypothalamus in the development of spontaneous (genetic) hypertension in rats.
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PMID:Changes in central catecholaminergic neurons in the spontaneously (genetic) hypertensive rat. 63 Jun 70

In human renal venous strips from normotensive and hypertensive patients, adrenergic- and nonadrenergic-induced contractions were elicited. The maximal amplitude of contractions remained unchanged whatever the mode of activation. However, in the hypertensive group the forces generated reached only about 20% of those in the normotensive group. Furthermore, preparations from hypertensive patients showed a reduced sensitivity for noradrenaline: the ED50 was shifted from 0.13 +/- 0.03 to 0.66 +/- 0.19 microgram/ml (p less than 0.01). This reduced sensitivity is discussed in connection with the pathogenesis of hypertension.
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PMID:Adrenergic and nonadrenergic activation of isolated human renal veins of normotensive and hypertensive patients. 63 Nov 49

Studies were performed in nine male patients with moderate hypertension. Treatment with metoprolol, 50--150 mg three times daily for 4--17 weeks, had no effect on the plasma level of glycerol, free fatty acids, triglycerides or glucose under basal conditions, neither in the supine nor in the upright position. Submaximal work, performed postprandially, increased plasma glycerol before medication but not during metoprolol, in spite of a marked increase in plasma noradrenaline. The work load employed caused no change in free fatty acids, triglycerides or glucose, neither before medication nor during metoprolol.
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PMID:Effect of metoprolol on blood glycerol, free fatty acids, triglycerides and glucose in relation to plasma catecholamines in hypertensive patients at rest and following submaximal work. 63 34

Several models of experimental hypertension are described (neurogenic, mineralocorticoid, renovascular and genetic hypertension). An activation of the sympathetic nervous system is seen in these situations (increases in sympathetic nervous discharge, in the synthesis of noradrenaline and in the level of plasma catecholamines). This activation may be connected with biochemical abnormalities within the medulla which have been noticed for catecholamines and serotonin. These medullary abnormalities could themselves depend on abnormalities situated at higher levels (hypothalamus). The factors which determine the central problem and their mechanism of action are still hypothetical (e.g. the direct effect of sodium on the brain, the effect of stress and the environment as well as genetically determined biochemical abnormalities of the central nervous system). In the case of essential hypertension in man, available data are limited to the levels of plasma catecholamines which suggest an increased sympathetic activity of central origin when these levels are elevated.
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PMID:[Arterial hypertension: the role of the central nervous system. II. Experimental and clinical study (author's transl)]. 64 71

Six-hydroxydopamine (6-OH-DA) was administered intraventricularly to 6-week-old and 5-month-old spontaneously hypertensive rats (SHR), and was administered into the spinal cord of 6-week-old SHR. Intraventricular administration of 6-OH-DA into 6-week-old SHR prevented the development of hypertension for at least 12 weeks; pressor response of the perfused hindquarters to noradrenaline was the same in 6-OH-DA-treated and vehicle-treated animals. Intraventricular administration of 6-OH-DA into 5-month-old SHR with established hypertension produced only a transient fall in blood pressure. Local injection of 6-OH-DA into the spinal cord produced a marked reduction only in spinal cord noradrenaline but did not affect the development of hypertension in SHR. These findings suggest that brain adrenergic neurons may participate in the development of hypertension in SHR but noradrenergic projections in the spinal cords are not essential for this process.
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PMID:Effects of intraventricular and intraspinal 6-hydroxydopamine on blood pressure of apontaneously hypertensive rats. 66 57

Urinary excretion of catecholamines, vanillylmandelic acid, and methoxycatecholamines was studied in 50 patients with renovascular hypertension. The urinary excretion of noradrenaline was increased in patients with elevated peripheral plasma renin activity and in those with elevated renal vein renin ratio in comparison with the patients with normal plasma renin activity. The urinary excretion of dopamine was diminished and vanillylmandelic acid increased in the entire group of patients with renovascular hypertension. In the investigated group, following sodium restriction, the mean urinary excretion of noradrenaline increased while dopamine excretion decreased. These results suggest that the increased sympathetic activity may play a role in the pathogenesis of renovascular hypertension.
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PMID:Urinary excretion of catecholamines and their metabolites in patients with renovascular hypertension. 73 71

1. The membrane properties and sensitivity to chemical substances of smooth muscle cells of the portal vein and pulmonary artery were studied in normotensive rats (Wistar Kyoto) and spontaneously hypertensive rats (Okamoto & Aoki) by the micro-electrode method. 2. The parameters of the membrane, i.e. resting membrane potential, the maximum rate of rise of the spike, space constant of the tissue and time constant of the membrane measured from the portal vein were the same in normotensive rats (less than 120 mmHg) and spontaneously hypertensive rats (greater than 165 mmHg). Similar results were also obtained from the pulmonary artery. Such findings indicate that the passive electrical properties of the vascular muscle membrane are not involved in the generation mechanism of hypertension. 3. In the portal vein the maximum slope of the membrane depolarization produced by tenfold increase in external K+ concentration expressed on a logarithmic scale was the same in normal and hypertensive rats (42 and 41 mV, respectively). These observations were confirmed by the effects of application of excess K+ on the pulmonary artery (48 mV in normal and 46 mV in hypertension). With a low concentration of K+, the membrane was depolarized to a greater extent in the portal veins than in the pulmonary arteries of both types of rats. Although the response to K+ differed in vascular muscles excised from the different regions, no functional difference was apparent between normotensive and hypertensive. 4. In both portal vein and pulmonary artery, the smooth muscle membrane of spontaneously hypertensive rats proved to be more sensitive to noradrenaline, i.e. depolarization of the membrane appeared with noradrenaline 10(-9) g/ml. in hypertensive but with 10(-8)g/ml. in normotensive rats. Depolarization block of the spike generation appeared at a slower concentration of noradrenaline in hypertensive rats. Sensitivity of the smooth muscle membrane to prostaglandin E2 in the portal vein was also higher in hypertensive rats. 5. The present results indicate that the only difference between normal and spontaneously hypertensive rats regarding smooth muscle cell membrane of the pulmonary artery and portal vein is increased chemical sensitivity in hypertensive rats, and the passive electrical properties of the membrane probably does not contribute to the generation of hypertension.
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PMID:Electrical property and chemical sensitivity of vascular smooth muscles in normotensive and spontaneously hypersensitive rats. 74 2

The pathogenic role of the sympathetic system in essential hypertension was evaluated by combined analysis of urinary and plasma catecholamine levels and pressor sensitivity to endogenous noradrenaline. The latter was estimated indirectly by the ratio between percentile changes in blood pressure and plasma noradrenaline following adrenergic neuronal blockade with the agent debrisoquine. In normal and mildly hypertensive (141/91 to 160/105 mm Hg) subjects, supine or upright plasma levels and excretion rates of noradrenaline correlated (p less than 0.01) with age and were comparable; no correlation was present in patients with moderate to severe hypertension (greater than 160/105 mm Hg) who tended to have supernormal noradrenaline levels under the age of 40 years. Adrenaline values were normal in essential hypertension. Pressor sensitivity to noradrenaline was comparable in normal and mildly hypertensive subjects (0.03 +/- 0.08 [SE] and 0.17 +/- 0.04, respectively) but increased (p less than 0.001) in moderate to severe hypertension (0.62 +/- 0.11). These findings suggest that moderate to severe essential hypertension may be maintained, at least partly, by the inappropriate association of normal plasma noradrenaline levels with increased noradrenaline pressor sensitivity. This may also provide a rational basis for the use of pharmacologic adrenergic inhibition in the treatment of moderate to severe essential hypertension.
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PMID:[Significance of noradrenaline in the pathogenesis of essential hypertension. Preliminary report]. 74 96


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