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

1. The autonomic and local control of the circumflex coronary bed evoked through acute rises in aortic pressure (aortic balloon inflation) was analysed in conscious, normotensive and hypertensive dogs in complete heart block with ventricles paced at 100 beats/min. 2. In normotensive dogs there was an initial rise (6-12 s) in circumflex conductance preceding a fall in conductance as aortic pressure increased and was sustained. The initial rise, but not the later fall, in circumflex conductance was partly due to a cholinoreceptor and partly due to alpha-adrenoreceptor mechanisms. Local constrictor mechanisms were responsible for the later fall in conductance. 3. The initial cholinoreceptor component of the rise in circumflex conductance is initiated through arterial baroreflex mechanisms. 4. The initial autonomic mechanisms regulating circumflex conductance appear to be absent in renal hypertension. 5. The absence of the transient autonomic rise in circumflex flow and conductance in response to rapid elevations in aortic pressure in certain forms of hypertension, e.g; during tachyarrhythmias and behavioural disturbances, may result in myocardial ischaemia when it is least appropriate.
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PMID:Baroreflex control of coronary conductance in normotensive and renal hypertensive conscious dogs with complete heart block. 107 46

1. We have compared the effect of central and peripheral administration of angiotensin II and (1-succinamoly-5-valine-8-phenylglycine)angiotensin II on blood pressure of male conscious unrestrained rats with normal blood pressure, and with spontaneous hypertension or chronic renal hypertension. 2. After central and peripheral injection of angiotensin II all rats exhibited a significant dose-related increase in blood pressure. 3. Administration of the analogue was without effect in normotensive rats. Ten-weeks-old rats with spontaneous hypertension showed a significant blood pressure decrease after central injection, but an increase after peripheral injection. This centrally induced decrease could not be observed in spontaneously hypertensive rats 14 weeks old. In these animals the analogue increased the blood pressure. In rats with chronic renal hypertension in contrast to peripheral injection, central administration decreased the pressure significantly. 4. Plasma renin activity was not changed after central injection of the analogue in normotensive rats. 5. These observations suggest the participation of the intrinsic brain isorenin-angiotensin system in central blood pressure regulation in these forms of experimental hypertension.
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PMID:Blood pressure response to central and peripheral injection of angiotensin II and 8-C-phenylglycine analogue of angiotensin II in rats with experimental hypertension. 107 54

1. The role of arginine-vasopressin in the pathogenesis of malignant deoxycorticosterone (DOC) hypertension of rats was investigated. 2. In rats with malignant DOC hypertension plasma arginine-vasopressin concentrations increased more than tenfold subsequent to volume depletion and a rise of serum osmolality. 3. The injection of a specific antibody serum for arginine-vasopressin caused a marked fall of blood pressure in rats with malignant DOC hypertension, whereas the injection of angiotensin II antiserum did not affect blood pressure. 4. In rats exhibiting a benign course of DOC hypertension plasma concentrations of arginine-vasopressin were increased threefold in comparison with normotensive control rats; the injection of an arginine-vasopressin antiserum induced a significant but small fall of blood pressure. 5. It is concluded that in the pathogenesis of malignant DOC hypertension arginine-vasopressin might play the role that the renin-angiotensin system plays in the pathogenesis of malignant renal hypertension.
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PMID:Vasopressin and malignant deoxycorticosterone hypertension in rats. 107 63

1. The angiotensin II antagonism by newly synthesized 8-C-phenylglycine analogues of [5-isoleucine]angiotensin II in different preparations was investigated in vitro and in vivo. 2. All analogues competitively inhibited the myotropic effect of angiotensin II on the isolated colon ascendens of the guinea-pig and the stomach of the rat. 3. In normotensive dogs, cats, rabbits, guinea-pigs and rats the blood pressure response to infused angiotensin II was inhibited by the antagonists. The angiotensin II-induced fall in renal blood flow in the dog was blocked during infusion of the analogues. Acute renal hypertension in rats was significantly decreased. Of conscious rats variously with normal blood pressures, spontaneous hypertension and chronic renal hypertension, only in the last group could a marked uniform fall in blood pressure be demonstrated. The central pressor effect of angiotensin II was also inhibited in conscious rats. 4. 8-C-Phenylglycine analogues of [5-isoleucine]-angiotensin II exhibit a specific antagonistic activity to endogenous and exogenous angiotensin II.
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PMID:Comparative pharmacology of new specific angiotensin antagonists. 107 69

The sympathetic nervous system has been postulated to play a role in the maintenance of renal hypertension. Permanent peripheral sympathectomy was performed by treating newborn rats for 21 days with guanethidine. Sympathectomy was confirmed by (1) relative insensitivity to tyramine, (2) lack of responsiveness to renal nerve stimulation, and (3) absence of dopamine-beta-hydroxylase immunofluorescence in renal blood vessels. Placement of a clip on the left renal artery led to the development of two-kidney renal hypertension. No differences were observed between the two-kidney renal hypertensive normal and sympathectomized rats; both had elevated plasma renin activity and vasodepression with angiotensin antagonists which were maintained up to nine weeks. Furthermore, in normal rats chronic beta-adrenergic blockade with propranolol caused no change in the development of the two-kidney renal hypertension. Similarly, no differences were seen in blood pressure, plasma renin activity, or response to antagonists between the one-kidney renal hypertensive (clip plus contralateral nephrectomy) normal and sympathectomized rats. Both showed sustained low renin hypertension up to 12 weeks. The absence of the peripheral sympathetic nervous system did not affect the development or maintenance of hypertension in either model of hypertension.
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PMID:Development and maintenance of renal hypertension in normal and guanethidine sympathectomized rats. 109 53

The effect of neonatal thymectomy on the degree and prognosis of hypertension and on the vascular lesions in rats with renal hypertension was studied. There were no differences between thymectomized and sham operated hypertensive rats. The degree of hypertension, the frequency of spontaneous death and heart infarcts were the same in both groups. The occurrence and degree of perivascular cell infiltrations, deposits of perivascular connective tissue and fibrinoid degenerations of the media were found to be the same in both the thymectomized and the sham operated hypertensive animals. The results do not support the assumption that delayed type immune reactions are important in the pathogenesis of hypertensive vascular disease in renal hypertensive rats.
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PMID:Influence of neonatal thymectomy on blood pressure and hypertensive vascular disease in rats with renal hypertension. 109 29

Information defining the renin-angiotensin-aldosterone axis as a control system concurrently regulating salt balance and blood pressure has been applied to examine the role of renin in the causation of experimental and clinical forms of renovascular and renal hypertension and thence to develop criteria for differentiating these entities. Experimantally there are two models of renovascular hypertension, one characterized by excess renin with reduced sodium (vasoconstrictor form) and the other by excess sodium with reduced renin (volume form). But with sodium depletion, the volume form switches to a vasoconstrictor form, illustrating how the two factors coordinate to maintain blood pressure. Human renovascular and renal hypertensions appear to be sustained by the same two mechanisms. Experimental and clinical studies both indicate that curable renal hypertension is in fact a renin-dependent vasoconstrictor hypertension. Three criteria, derived from four renin measurements, identify this situation: (1) Hypersecretion of renin is reflected by a high peripheral level when referenced against sodium excretion. (2) Lacteralization of renin secretion with contralateral suppression rules out occult bilateral disease. It is indicated by V-A = 0 from the uninvolved kidney. (3) A third criterion, (V-A)/A greater than 48 per cent from the ipsilat-eral kidney, identifies renal ischemia. These three criteria, when taken together in a combined scoring analysis, provide high precision in identifying the patient with the vasoconstrictor form of renal hypertension that is potentially reversible by appropriate surgery. Absence of these criteria identifies hypertension associated with either occult or overt bilateral renal disease. In these patients, the volume factor often predominates and is expressed by some suppression of plasma renin levels. Here, removal of renal tissue is contraindicated. Corroborative evidence to support these three criteria can be developed from the blood pressure response to angiotensin blocking drugs or to anti-renin therapy with propranolol. Thus in all of these renal hypertensions, the vasoconstrictor and volume factors can be identified using renin measurements and pharmacologic interventions.
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PMID:New concepts of the renin system and of vasoconstriction-volume mechanisms. Diagnosis and treatment of renovascular and renal hypertensions. 109 53

The study of hypertension resulting from procedures devised to modify renal function in diverse ways has been pursued intensively in the past forty years and has contributed greatly to the understanding of hypertensive processes in man. Such procedures have included partial or complete removal of renal tissue, interference with the renal circulation and the administration of sodium and hormones promoting the tubular reabsorption of sodium. From all these studies, certain basic conclusions can be drawn. The fundamental mechanism involved in all forms of renal hypertension appears to be an alternation in the relationship between renal perfusion pressure and sodium and water excretion. The probable way in which this fundamental mechanism operates is outlined. The kidney itself is susceptible to the effects of hypertension and changes take place within it which then contribute a renal element to the hypertension whatever its primary cause.
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PMID:Experimental renal hypertension. 110 32

The history of the development of ideas on the cause of renal hypertension is first discussed. Growth of knowledge of renin and angiotensin from 1898 to the present is shown to depend upon better and more specific assays for each part of the system, which has enabled knowledge of the role of the renin-angiotensin system in various forms of hypertension to be assessed accurately. The difficulties of assessing varying levels in relation to their biological effect is stressed and the importance of the use of blockers of both renin and angiotensin is shown to mark a very large advance in the study of various forms of renal hypertension where there is a complicated relationship, still ill-defined, between renin, angiotensin, sodium and body fluid volumes.
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PMID:The place of renin in the mechanism of hypertension in chronic renal disease. 110 33

The role of prostaglandin A (PG A) in the pathogenesis of renal hypertension has been studied. The concentration of endogenous PG A was measured in the peripheral plasma by radioimmunoassay in patients with chronic renal disease and in control subjects. The mean plasma concentration of PG A1 equivalents was as follows: 1. normotensive healthy volunteers (n=23): 115 +/- 15 pg/ml 2. patients in terminal renal failure on regular hemodialysis a) anephric patients (n=6): 51+/- 21 pg/ml b) patients retaining their own kidneys, all but one with hypertension (n=9): 231 +/- 51 pg/ml (P less than 0.01 versus control) 3. patients with chronic renal disease a) with hypertension (n=7): 204 +/- 60 pg/ml (P less than 0.01 versus control) b) without hypertension (n=11): 136 +/- 30 pg/ml. Renal hypertension was associated with high levels of PG A in peripheral blood. This increase is probably a secondary adaptative mechanism for the excretion of a greater fraction of the glomerular filtrate at a lower blood pressure. PG A may represent a circulating "antihypertensive hormones".
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PMID:Prostaglandins and hypertension in chronic renal diseases. 110 34


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