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

The renin-angiotensin system and dietary sodium have been repeatedly implicated in the pathogenesis of pregnancy induced hypertension (PIH). Mechanisms responsible for increased vascular responsiveness to angiotensin II (A-II) observed in PIH are not completely understood. Plasma A-II levels and blood pressure are functions of sodium balance in the non-pregnant state, but less is known about their relationship during gestation. Plasma levels of A-II increase in normal pregnancy, but the reported levels of this pressor substance circulating in subjects with PIH are in conflict. The pregnant rabbit demonstrates several conditions similar to those found in pregnant human subjects. We used this model to study the effects of dietary sodium manipulation on plasma levels of A-II and mean arterial pressure during late pregnancy in 30 chronically prepared New Zealand white rabbits. The animals were 24 to 28 days gestation (term 30 +/- 1 day). All animals were maintained on 1 of 3 diets for 8 days prior to operation and for the duration of the investigation: 10 were fed Purina regular chow (0.4% sodium), and permitted to drink 0.9% saline, 10 were fed trace-sodium diet (Purina 5881-R) and deionized water ad libitum; and 10 were continued on tap water and regular rabbit chow (0.4% sodium) and served as controls. Urines were collected for 24 hours prior to surgery for sodium determination. An indwelling catheter was placed in the carotid artery for blood pressure recording and blood sampling. After a 20 minute stabilization period, mean arterial pressure was repeatedly recorded and blood samples were obtained for determination of A-II levels and sodium concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma angiotensin II and blood pressure changes during dietary sodium manipulation. 651 60

DOCA-salt hypertension was produced in 10 male 10-week-old normotensive Wistar-Kyoto (WKY) rats receiving deoxycorticosterone acetate (DOCA; 100 mg/kg, subcutaneous pellet) and 1% NaCl drinking water and was compared with data from 10 age- and sex-matched WKY receiving normal tap water (C). These data were also compared with spontaneously hypertensive (SHR) rats similarly treated. After 10 weeks on these programmes, systemic and regional haemodynamics were determined in conscious rats using microsphere techniques. DOCA-salt treatment increased mean arterial pressure (MAP), total peripheral resistance index (TPRI), cardiac and renal weights in both WKY and SHR. In contrast to SHR (C), the SHR (DOCA) demonstrated more severe MAP elevation (204 +/- 4 versus 185 +/- mmHg; P less than 0.01), more severe systemic and regional (especially renal) vasoconstriction, and malignant vasculitis associated with azotaemia and hyperuricaemia. The hyperuricaemia was related inversely to renal blood flow (r = -0.74; P less than 0.01) and directly to renal vasoconstriction (r = 0.65; P less than 0.05) in SHR (DOCA). These data suggest that in both WKY and SHR, DOCA and salt produced marked cardiovascular changes and SHR rats developed malignant hypertension.
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PMID:DOCA-salt induced malignant hypertension in spontaneously hypertensive rats. 653 May 37

We present the case of a 64-year-old alcoholic who had suffered two episodes of hemorrhage from esophageal varices. For control of variceal hemorrhage, he underwent a distal splenorenal shunt. His immediate postoperative course was complicated by the development of marked ascites and intermittent episodes of encephalopathy. Routine postoperative angiography was performed after 4 months and demonstrated a fistula between the left gastric artery and vein. Patency of the shunt was demonstrated by direct percutaneous splenoportography. Two months after this admission, the patient was readmitted with the complaints of anorexia and nausea. Marked encephalopathy was noted. Eight hours following admission, he developed acute abdominal distention and hypotension. An abdominal tap revealed bloody fluid, and the patient was immediately prepared for transport to the operating room. He suffered cardiac arrest during transport, and all efforts at resuscitation were unsuccessful. Although a postmortem examination was not performed, it is suspected the arteriovenous fistula resulted in severe portal venous hypertension leading to intraperitoneal rupture of one of the affected veins, producing a massive hemoperitoneum.
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PMID:Left gastric arteriovenous fistula after selective distal splenorenal shunt. 660 11

It is uncertain whether increased arterial pressure alone or increased arterial pressure combined with some other factor is responsible for the development of malignant-phase hypertension. Our object was to test this comparing two groups of rats with hypertension of different mechanism but of similar duration and degree. Two experiments were done in hypertensive rats. In the first blood pressure was measured in the tail, in the second by intra-arterial catheter and pressure transducer. In the first, hypertension was produced in 30 male Sprague-Dawley rats by unilateral nephrectomy followed by thrice-weekly injections of deoxycorticosterone (12.5 mg) and substitution of 1% NaCl and 0.2% KCl for their drinking water. After four weeks 28 rats survived and systolic blood pressure had risen to 220 mmHg. The survivors were paired by blood pressure and randomly allocated either to continued DOC and salt or to a regime in which DOC was stopped and tap-water was substituted for the NaCl-KCl solution (post-DOC rats). Blood pressure remained similar in the two groups thereafter, but in every case it was the DOC-salt animal of the pair which died first. Fibrinoid arteriolar lesions of malignant-phase hypertension were significantly commoner in DOC-salt animals and, before death, they had more pronounced features of microangiopathic haemolytic anaemia. The second experiment was the same in design as the first except that two weeks after randomization the similarity of blood pressure was confirmed by measurement of intra-arterial pressure in eight pairs of DOC-salt and post-DOC rats. We conclude that increased arterial pressure is not the only factor influencing development of malignant-phase hypertension.
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PMID:Similar blood pressure but different outcome in rats with DOC and post-DOC hypertension. 668 Oct 45

Increased sympathetic nervous system activity and vasopressin release has been demonstrated in established DOCA-salt hypertension in the rat. To determine the importance of these mechanisms in centrally-mediated pressor responses in this model of hypertension, both awake rats and rats anaesthetised with urethane were given intracerebroventricular injections of carbachol. The systolic blood pressure after implanting a silicon rubber mould containing DOCA, and with subsequent substitution of 1% saline in tap water, increased from 112 +/- 3 mmHg to a stable 188 +/- 7 mmHg by the end of 4 weeks, measured using a tail-cuff method. The blood pressure consistently became elevated when carbachol was injected into the cerebral ventricles of awake rats. Of the three groups of normotensive rats (NTR), sham-operated rats (SHAM) and DOCA-salt hypertensive rats (DOCA), the magnitude of the pressor phase was largest in the DOCA rats. The heart rate in all three groups of rats decreased similarly. When the rats were later anaesthetised with urethane to allow recording of abdominal sympathetic nerve activity, the carbachol injections caused biphasic blood pressure responses and sympathetic nerve discharge consisting of initial vasodepression and sympathetic nerve inhibition of short duration. This was followed by a sustained pressor phase accompanied by a corresponding increase in sympathetic nerve activity. The magnitude of the pressor response was again larger in the DOCA than in the SHAM rats. Spinal section abolished the initial depressor phase but did not much affect the sustained pressor phase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Centrally-induced vasopressor responses to carbachol are augmented in DOCA-salt hypertensive rats. 669 39

Micropuncture and/or morphologic studies were performed in seven groups of uninephrectomized (UNX) adult male Munich-Wistar rats. Control groups 1, 3, and 6 received standard (24% protein) chow and tap water. Groups 2, 4, and 5 received weekly injections of desoxycorticosterone pivilate (DOC) and 1% saline for drinking, groups 2 and 4 were fed standard chow, and Group 5 a diet containing 6% protein. Group 7 received DOC, salt, and standard chow for 3 wk followed by withdrawal of DOC and salt for an additional 6 wk. 10-14 d after UNX, groups 1 and 2 exhibited similar single nephron glomerular filtration rates (SNGFR) and initial glomerular plasma flow rates (QA). Group 2 had higher mean arterial pressure (AP) and glomerular capillary hydraulic pressure (PGC) than group 1. 3-4 wk after UNX, group 4 exhibited further elevations in AP and PGC as compared with groups 2 and 3. SNGFR and QA were similar in groups 3 and 4, but these average values were greater than typical for normal rats. Group 4 also demonstrated increased urinary protein excretion. Morphologic evaluation of glomeruli in groups 2 and 4 revealed mesangial expansion and focal intraglomerular hemorrhage whereas glomeruli of groups 1 and 3 were essentially normal. Values for AP and PGC in group 5 were not different than group 3 but significantly lower than group 4. QA and SNGFR were lower in group 5 (low protein) than in groups 3 and 4. Furthermore, proteinuria and glomerular structural lesions were abolished in group 5. Morphologic studies performed in groups 6 and 7 showed that early DOC-SALT lesions progress to focal glomerular sclerosis. These studies suggest that continued elevations in glomerular capillary flows and pressures predispose to glomerular injury in this model of systemic arterial hypertension.
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PMID:Hemodynamic basis for glomerular injury in rats with desoxycorticosterone-salt hypertension. 671 46

The ability of propranolol, a beta-adrenergic blocking agent, to decrease blood pressure and inhibit the development of hypertension was assessed in spontaneously hypertensive rats (SHR). Oral propranolol was administered via drinking water to SHR and age matched normotensive control (WKY) groups beginning at conception, birth, three, six, or nine weeks of age. Controls for all groups were given tap water. Propranolol treatment was withdrawn from all groups at twelve weeks of age. A comparison of developmental parameters such as water consumption, weight gain and survival showed no differences between SHR and WKY or between SHR with propranolol vs WKY with propranolol. Systolic blood pressures and heart rates were monitored non-invasively from seven to sixteen weeks of age. There was a variable reduction in SHR blood pressures during propranolol treatments starting at 6 weeks of age or earlier, but when propranolol treatment was withdrawn, SHR blood pressures increased as did SHR without propranolol treatment. In SHR offspring who were exposed to propranolol through fetal and neonatal development and whose sires and dams were pretreated with propranolol, the development of high blood pressure was inhibited. Blood pressures indicated that this group did not develop hypertension for up to four weeks after propranolol was withdrawn even though heart rate returned to normal. Based upon these findings, a critical period during SHR development was defined during which development of hypertension can be inhibited by propranolol.
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PMID:Propranolol can inhibit the development of hypertension in SHR. 674 42

To clarify the functions of the agranular cells in the polar cushion of the juxtaglomerular apparatus, the effects of drinking 1% NaCl or eating a diet containing 8% NaCl were examined on the numbers of granular and agranular cells in the polar cushions, the kidney weights, and the blood pressures of male Sprague-Dawley rats after uninephrectomy. Only 11.8% of the cells in the polar cushions of control rats in this study were granular; hence, 88.2% of the cells were agranular. After uninephrectomy of rats on a normal diet with tap water, the maximal increase in relative weight of the remaining kidney occurred within 2 weeks, and the degree of hypertrophy was estimated as 64%. Rats with a high salt intake after uninephrectomy had a similar increase, indicating that a high salt intake after uninephrectomy did not affect the degree of hypertrophy of the remaining kidney. The mean juxtaglomerular cell count (JGCC) showed moderate increases 2 weeks after uninephrectomy. Drinking 1% NaCl for 2 weeks after uninephrectomy produced about twice as much increase in the JGCC. Maximal initial increases in JGCCs occurred at 2 weeks, well before an increase in blood pressure. Drinking 1% NaCl had no significant effect on blood pressure within 2 weeks, but there was a definite hypertension at 8 weeks, with no further increase in JGCC. On an 8% NaCl diet hypertension developed between 8 and 16 weeks, when the JGCC was greater than previous levels. Clipping the renal artery of a solitary kidney produced hypertension but no increase in JGCC within 2 weeks. Uninephrectomy lowered the mean granular cell count, and drinking saline lowered it even more. Hence, the proliferation involved agranular cells. In summary, excessive NaCl intake was associated with a rapid proliferation of agranular cells which was maximal at 2 weeks and occurred before any significant increase in blood pressure. This suggests that the agranular cells in the polar cushion of the juxtaglomerular apparatus are concerned more directly with sodium chloride metabolism than with blood pressure regulation.
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PMID:Effects of excessive sodium chloride on the juxtaglomerular apparatus and blood pressure of uninephrectomized rats. 686 35

Balances of sodium, potassium, and water were studied in the growing male pig as hypertension developed in response to subcutaneous implantation of deoxycorticosterone acetate (DOCA). Serum sodium, potassium, deoxycorticosterone (DOC), aldosterone, and plasma renin activity (PRA) were determined. These variables were observed in a total of 10 experimental and nine control pigs. All animals were uninephrectomized and fed a diet of Purina Pig Chow and tap water ad libitum. No salt was added to the food or water. Serum DOC levels rose dramatically on the day of the implantation, then gradually declined but remained approximately 10 times greater than control levels 40 days after implant. Plasma renin activity was suppressed rapidly and completely, whereas aldosterone fell only slowly to about half its control value. Sodium retention was maximum during the first 24 hours. Therefore an "escape" process became operative, causing sodium balance to return to normal after the third day, at which time the major rise in arterial pressure occurred. A marked increase in water turnover (intake and output) also began after the third day and persisted throughout the experimental period. Water balance remained normal during this period of increased turnover. Hypokalemia developed in the absence of kaliuresis, suggesting that potassium moved into the cells. Except for the potassium retention, these changes parallel the abnormalities seen in other states of mineralocorticoid excess.
Hypertension
PMID:Electrolyte and hormonal effects of deoxycorticosterone acetate in young pigs. 699 59

We studied the effects of dietary sodium on the magnitude of hypertension in sinoaortic denervated (SAD) rats. Groups of SAD rats and sham operated (SO) controls drank tap water and received chows with different amounts of sodium: low (0.08%), regular (0.4%), high (3%) or very high (7%) sodium; other groups, some after unilateral nephrectomy, received regular chow and 1% saline to drink. These various sodium regimens were started before operations and were continued for at least 12 weeks after SAD and SO. Weekly systolic tail-cuff pressures of SAD rats were significantly higher throughout the 12 week postoperative period than those of SO rats regardless of sodium regimen (p less than 0.05 to less than 0.01). Analysis of variance indicated no significant differences between pressures of SAD rats on regular or low sodium chows and those receiving any of the high sodium regimens. When SAD rats were switched from regular to high sodium diets no significant change was induced in systolic pressures. We then examined renal sodium excretion in response to oral sodium loading or to intravenous saline infusion in groups of SAD and SO rats. Both types of studies revealed that SAD rats excreted the extra sodium significantly faster than SO rats. We conclude that hypertension induced by SAD is not dependent on the amount of sodium in the diet and that the magnitude of hypertension is not increased by chronic high sodium intake. The rapid excretion of sodium suggests SAD rats have an enhanced sensitivity to activation and/or to effects of neural and/or humoral factors affecting renal sodium excretion.
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PMID:Blood pressure and sodium excretion in the sinoaortic denervated rat during chronic high and low sodium intake and acute sodium loading. 707 99


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