Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma kallikrein releases bradykinin when activated by gram-negative septicemia or irreversible hemorrhagic shock. Pancreatitis releases glandular kallikrein causing hypotension and increased vascular permeability. Bradykinin in the brain produces hypertension. Renal kallikrein is released by high arterial pressure, vasodilators, low doses of noradrenaline, angiotensin II, mineralocorticoids and rapid volume expansion. It has a biphasic relation to sodium excretion. In essential hypertension, kallikrein release into the blood and urine is low and facilitates hypertension. High renin in Bartter's syndrome is balanced by high PGE and kallikrein without hypertension.
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PMID:Kallikrein, kininogen and kinins in control of blood pressure. 37 13

1. The effects of atenolol on diurnal blood pressure control, heart rate and plasma catecholamines were studied in nine hypertensives, six of whom also received diuretics. The patients completed a double-blind trial in which the effects of once and twice daily administration of atenolol were compared with placebo. 2. Atenolol (100 mg) given once a day produced significant reduction in diurnal blood pressures recorded at home but the effect was slightly less than either 50 mg given twice a day or 200 mg once a day. 3. Effects on heart rate and blood pressure were seen within 36 hours of the first dose, and were near maximal at 72 hours. After cessation of the drug, mean resting heart rate increased gradually and reached pre-treatment levels five days later, suggesting strong tissue binding of atenolol. Blood pressure increased more slowly over 8--10 days. 4. Plasma noradrenaline levels were increased at rest with atenolol. This argues strongly against the antihypertensive effect of atenolol being due to a reduction of sympathetic nerve activity. 5. Once daily administration of atenolol in this group of patients with mild hypertension produced satisfactory diurnal blood pressure control and beta blockade without "rebound" hypertension on cessation of therapy.
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PMID:Home blood pressure monitoring and changes in plasma catecholamines during once or twice daily treatment with atenolol in patients with mild hypertension. 38 23

The renin-angiotensin-aldosterone system, electrolyte and water balance, body fluid, and neurogenic tone and reactivity of the vasculature were studied in hypertension induced in uninephrectomized rats by repeated injection of renin-rich kidney extract and 1% saline drinking. The control rats were injected with physiological saline. Various measurements were made in conscious rats on the 10th day of the treatment. As compared with the control, plasma renin concentration and serum sodium increased significantly, while plasma aldosterone and renal excretory function did not differ. Blood volume (BV) expressed as per body weight increased significantly, but absolute BV, absolute or body weight-related plasma volume and hematocrit were not significantly different. The hypotensive effect of 1-Sar-8-Ile-angiotensin II was negligible 12 hours after the preceding injection of kidney extract. It was small but significant 1 hour after the injection. Increase in water turn-over and fractional sodium excretion occurred during the development of hypertension. Spironolactone did not significantly modify the developmental course. We observed increased depressor response to hexamethonium and increased reactivities to noradrenaline and angiotensin II (A II); these response curves relatively resembled those of spontaneously hypertensive rats. Hypertensive vascular changes were seen in the kidney and heart by histology. Thus, it was suggested that a direct vascular action of A II played a partial role in this hypertensive process while aldosterone played little role. The significance of BV increase and possible contribution of A II's other actions were discussed.
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PMID:Pathophysiological studies on hypertension induced in rats by kidney extract and salt. 39 83

1. Using the xenon-133 washout technique, the renovascular response to intrarenal infusions of 3 and 30 mumol/min noradrenaline in four baboons with dietary-induced hypercholesterolaemia was measured. 2. The degree of reduction in cortical blood flow rate during an intrarenal infusion of 3 mumol/min noradrenaline in the four hypercholesterolaemic baboons was not significantly different from that in normocholesterolaemic baboons. However, a significant difference in the degree of reduction in cortical blood flow rate was found with the 30 mumol/min noradrenaline infusion (P less than 0.05). 3. The mean arterial blood pressure of the four animals was significantly higher (P less than 0.001) than the mean blood pressure in baboons used in this laboratory for other experiments. 4. These results have shown that baboons with dietary-induced hypercholesterolaemia have an enhanced renovascular sensitivity to exogenous noradrenaline. However, the possibility that this enhanced sensitivity was due to the associated hypertension cannot be excluded.
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PMID:Renovascular hypersensitivity to noradrenaline in dietary-induced hypercholesterolaemia in baboons. 41 88

In 10 patients with chronic autonomic failure the clinical features and cardiovascular reflexes were correlated with the pressor responses to intravenous noradrenaline and tyramine. In all patients there was an exaggerated response to noradrenaline but a normal or only mildly exaggerated response to tyramine. Patients with lack of sinus arrhythmia and by implication baroreceptor reflex loss had greater responsiveness to pressor drugs than patients with preservation of this reflex. The responses to tyramine infusions imply that there must be sufficient noradrenaline released at defective sympathetic endings for a pressor response to occur. However, the lack of rise of plasma noradrenaline following tyramine, except in the patients with pure autonomic failure, clearly separates these responses from those of normal subjects. These results can be explained by the presence of lesions of both central and peripheral sympathetic pathways in patients with chronic autonomic failure and multiple system atrophy or Parkinsonism. The peripheral lesion, which is incomplete, may consist of replication of the receptors so causing supersensitivity with a duration of response that is little prolonged. The peripheral defect in the two patients with pure autonomic failure was found to be more complex and the prolonged response in one of these patients suggests the possibility of defective re-uptake or metabolism of noradrenaline. Clearly further study of the defects of sympathetic endings is required, including the use of other techniques such as catecholamine fluorescence. The extreme supersensitive responses underline the need for blood pressure monitoring during pressor drug studies prior to treatment, if the hazards of recumbent hypertension are to be avoided.
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PMID:Defective cardiovascular reflexes and supersensitivity to sympathomimetic drugs in autonomic failure. 42 28

The adrenaline content of specific brain stem areas was decreased in young (4 week-old) but not in adult (14 week-old) SHR. Some of these areas also showed increased PNMT activity, indicating a possible enhanced release or metabolism of adrenaline early in the development of the hypertension. Dopamine and noradrenaline levels, on the contrary, were not changed either in young or adult animals. Administration of a PNMT inhibitor to adult SHR resulted in a decrease of the blood pressure in SHR to control levels. These observations support the hypothesis of a participation of adrenergic mechanisms in the development of genetic hypertension, and indicate the possibility for the use of PNMT inhibitors as hypotensive agents.
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PMID:Adrenaline levels in brain stem nuclei and effects of a PNMT inhibitor on spontaneously hypertensive rats. 42 91

Knowledge of the vesicular origin of circulating dopamine beta-hydroxylase (DbetaH) is indispensable for any attempts to explain the parallelism or lack of it between circulating enzyme and catecholamines as they may relate to physiological stress, forms of hypertension, neurological disorders, and the response to pharmacological agents. The present study represents an effort to evaluate and to place in proper perspective data based on the DbetaH activity found in the region of the light vesicle peak of noradrenaline (NA), which is used as a quantitative measure of a population of small terminal vesicles. Distributions of vesicles and subvesicular components are compared with DbetaH and NA in sucrose-D2O density gradients used to prepare relatively pure fractions of large dense cored vesicles (LDV) from bovine splenic nerve. Although NA in sedimentable particles of the light vesicle peak is likely to be a valid measure of a small vesicle population, the following is demonstrated: (1) A substantial fraction (25%-37%) of the total sedimentable DbetaH activity can be proven to distribute in the region of the light vesicle peak from a tissue with an insignificant small vesicle population. Based on studies of vesicles from sequential nerve segments, this enzyme activity probably corresponds to a population of "immature" LDV which are undergoing axoplasmic transport and have not synthesized their full complement of transmitter. (2) Physical lysis which depletes the matrix of LDV causes redistribution of DbetaH activity from the heavy vesicle peak into the region of the light vesicle peak. Analogously, DbetaH associated with exocytosed LDV and retrograde transport particles is also likely to contaminate the region of the light vesicle peak. (3) Based on available data, it can be calculated that each small dense cored vesicle could contain only 0.1-0.5 molecules of DbetaH and that a contamination of only 0.016% LDV can account for all of the DbetaH reported to occur in the light vesicle peak of normal rat vas deferens preparations.
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PMID:Dopamine beta-hydroxylase distribution in density gradients: physiological and artefactual implications. 45 40

In severe cases of tetanus an overactivity of the sympathetic nervous system has been postulated because of the clinical symptoms including hypertension, fluctuating blood pressure, tachycardia, tachyarrhythmia and peripheral vasoconstriction. In the present study the involvement of the sympathetic nervous system in tetanus was investigated by serial determinations of plasma adrenaline (A) and noradrenaline (NA) in 2 patients who developed severe symptoms of tetanus and the characteristic cardiovascular disturbances. Sustained high circulating levels of NA and A could be observed indicating a prolonged overactivity of the sympathetic nervous system. In one case, the elevation of the NA level in plasma persisted until the disturbances of the motor nervous system ceased. In a third case of tetanus without cardiovascular abnormalities, the plasma NA and A only increased slightly on a few occasions. The results demonstrate that an overactivity of the sympathetic nervous system can complicate the course of severe tetanus.
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PMID:Dysfunction of the sympathetic nervous system in tetanus. A study of 3 cases. 45 74

Plasma noradrenaline (PNA) concentrations were measured in 38 subjects aged 13-23, who were followed up for two to four years after an initial blood-pressure (BP) reading of 140/90 mm Hg or over was obtained, and in 39 age-matched controls from the same open population. Subjects who were hypertensive when the PNA concentration was measured had a significantly higher concentration (351 +/- SE 26 pg/ml) compared with their controls (248 +/- 29 pg/ml). Furthermore, in those subjects in whom the mean arterial pressure decreased by under 5% during the follow-up period the mean concentration was 363 +/- 27 pg/ml, compared with 271 +/- 29 pg/ml in their controls. PNA concentrations and systolic BP were positively correlated. A positive association between PNA concentrations and age was observed in the controls but not the subjects with hypertension, owing to the higher concentrations in younger hypertensive subjects.
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PMID:Raised blood pressure and plasma noradrenaline concentrations in teenagers and young adults selected from an open population. 46 4

Hypertension was induced in rats (Hebrew University strain) by three different procedures: (1) deoxycorticosterone acetate (DOCA)--salt treatment; (2) unilateral renal artery clip or (3) chronic salt-loading. Noradrenaline (NA) and dopamine (DA) distribution in different brain areas was assayed following induction of hypertension. NA content increased significantly in various areas: the increase of NA in the pons-medulla was common to all procedures inducing hypertension. NA content increased also in the mesencephalon, the hypothalamus and the rest of the forebrain (DOCA--salt hypertension), in the mesencephalon, the hypothalamus and the cortex (in renal clip hypertension). No significant changes in DA content were observed in any region of the brain following induction of hypertension by the three different methods. In two substrains, selected from the Hebrew University strain, for their respective sensitivity (H) or immunity (N) to hypertension induced by DOCA--salt treatment, there were no significant increases in NA or DA in any part of the brain following DOCA--salt treatment. Comparison of NA concentrations in these strains showed that NA was significantly higher in the pons-medulla of the untreated N strain rats than in the medulla of untreated H strain or in untreated rats of the original strain (Hebrew University). A model is presented suggesting that central NA-containing neurons plays a major role in controlling hypertension.
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PMID:Experimental hypertension and catecholamine distribution in the rat brain. 46 31


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