ISSN:0194-911X    

出版商:OVID    

年代:1985

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

The significance of the erythrocyte abnormalities described in rats and humans with spontaneous hypertension is far from clear. This study, in two highly inbred strains of rats, was designed to evaluate whether these abnormalities are primary and thus genetically related to hypertension. The Milan hypertensive strain (MHS) and its normotensive control strain (MNS) were used to carry out two types of experiments. In two groups of lethally irradiated (MHS × MNS) F, hybrids, bone marrow from MHS or MNS was transplanted. The differences in red cell function between the recipients of bone marrow from MHS and recipients of bone marrow from MNS were similar to those existing between the parental donor MHS and MNS: Na+-K+cotransport was increased (p < 0.02) and intracellular Na+content (p < 0.05) and cell volume (p < 0.02) were decreased in MHS. The same pattern was observed when this experiment was repeated in different groups of F, hybrids. In individuals of the segregating F2population, obtained by crossing the (MHS × MNS) F1hybrids, there was a positive correlation (p < 0.001) between the red blood cell Na + -K+cotransport and the mean blood pressure. These results indicate that the erythrocyte abnormalities may well be genetically associated with the primary cause of spontaneous hypertension in rats. Because of the many similarities demonstrated when young prehypertensive MHS or humans prone to develop hypertension are compared with their respective controls, it is possible that the findings described here in rats are relevant to human essential hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

To determine whether age-related changes in salt preferences occur over the lifespans of spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY), the same animals of each genotype were tested as juveniles, and as young and older adults. Taste preference ratios for NaCl and KCI, at concentrations from 0.001 to 1.0 M, were calculated using 24-hour, two-bottle preference tests of each salt versus distilled water. Genotype exerted a significant effect on preference for both NaCl and KCl (p < 0.0005). At each age and across concentrations, SHR had consistently higher preferences than did WKY. Few marked, age-related changes in overall preference for NaCl were noted within either strain, but juvenile and older adult SHR and WKY exhibited stronger preferences than did young adults for the higher concentrations of NaCl below the rejection threshold (p < 0.001). Statistical age by concentration preference trends for KCI were similar to those for NaCl in SHR. Young adult WKY, however, had a significantly lower rejection threshold for that compound than did juveniles and older adults (p < 0.001). These results indicate that genotype, age, salt type, and salt concentration can interact to influence salt preference in hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

Increased sympathetic outflow from the central nervous system to the periphery may contribute to the initiation of hypertension in spontaneously hypertensive rats (SHR). As this alteration in sympathetic activity may be mediated in part by α-adrenergic receptors in the central nervous system, the current study examined aradrenergic receptors in various brain areas of SHR and normotensive Wistar-Kyoto control rats (WKY). The α1-adrenergic receptor number and apparent affinity constants of brain sections of both young prehypertensive animals (4 weeks old) and mature hypertensive animals (12 weeks old) were studied with the a,-adrenergic receptor antagonist [3H]WB-4101 to label the α-adrenergic receptor. Five brain regions were studied: rostral hypothalamus, caudal hypothalamus, locus ceruleus, nucleus tractus solitarius, and frontal cortical poles. In comparison to normotensive controls, mature hypertensive rats had a significantly greater density (p < 0.05) of the aradrenergic receptors in the rostral hypothalamus (+ 11%), caudal hypothalamus (+ 25%), and frontal cortical poles (+ 20%). Significantly greater (p < 0.05) aradrenergic receptor density was found in the rostral hypothalamus (+ 27%), caudal hypothalamus (+ 60%), and locus ceruleus (+ 39%) of the young prehypertensive SHR compared with age-matched WKY. These results indicate the presence of altered adrenergic receptor systems in the brains of genetically hypertensive animals and suggest that changes in the receptor systems take place during establishment of the hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

Several inbred lines of rats were produced from noninbred stock of Dahl salt-sensitive (S) rats, and several inbred lines were also produced from noninbred stock of Dahl salt-resistant (R) rats. There were significant differences (p < 0.001) in blood pressure response to a high salt diet among the inbred S lines produced, which indicates that the original S stock obtained from Brookhaven Laboratories is not genetically homogeneous. There were no significant differences in blood pressure among the inbred R lines produced. One inbred strain of S and one inbred strain of R with the appropriate blood pressure responses were ultimately brother-sister mated for more than 20 generations. These inbred strains were called S/JR and R/JR respectively. Fulminant hypertension and marked vascular and renal lesions developed in the S/JR after 3 to 4 weeks on a high salt (8% NaCI) diet, and all S/JR were dead within 8 weeks on the high salt diet. In contrast, R/JR survived well on a high salt diet, and hypertension or vascular and renal lesions did not develop. Hypertension and associated vascular and renal lesions developed in S/JR on a low salt diet (0.4% NaCI), but this took 3 to 4 months. These characteristics are similar to those originally reported by Dahl for his noninbred, continuously selected stocks. The R/JR were found to have mild hydronephrosis at 4 months of age, which probably is genetically determined and which may have been fixed inadvertently in the strain during inbreeding. An age-related, strain-specific polymorphism in a stomach pepsinogen is described in the inbred S/JR and R/JR, which we believe can be used as a biochemical marker for the strains.

ISSN:0194-911X    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

The effects of intracerebroventricular (i.c.v.) administration of 0-adrenergic receptor antagonists (d, l-propranolol or timolol, 30 μg in 2 μL of isotonic saline) on the increased renal sympathetic nerve activity and decreased urinary sodium excretion (UNaV) responses to stressful environmental stimulation (air jet to head) in conscious spontaneously hypertensive rats (SHR) were examined. Before i.c.v. d, l-propranolol or timolol, air stress increased renal sympathetic nerve activity (68% from 10.6 ±2.1 and 63% from 8.2 ± 0.9 integrator resets/min respectively). In contrast, after i.c.v. d, l-propranolol or timolol in the same conscious SHR, air stress had no effect on renal sympathetic nerve activity (+ 7% from 8.1 ± 1.7 and +7% from 5.5 ± 1.0 integrator resets/min respectively). Air stress decreased UNaV in conscious SHR given i.c.v. saline vehicle (25% from 2.8 ± 0.5 μEq/min/100 g body weight), but had no effect on effective renal plasma flow or glomerular filtration rate. In contrast, after i.c.v. d, l-propranolol or timolol, air stress had no effect on UNaV (0% from 2.8 ± 0.5 and +9% from 3.3 ± 0.3 μq/min/100 g body weight respectively). Mean arterial pressure increased similarly during air stress with i.c.v. saline-vehicle or β-adrenergic receptor antagonists. Intravenous administration of the same doses of d, l-propranolol or timolol did not prevent the increased renal sympathetic nerve activity or decreased UNaV responses resulting from air stress. These results suggest that central nervous system β-adrenergic receptors mediate the increased renal sympathetic nerve activity and decreased UNaV responses resulting from stressful environmental stimulation in conscious SHR.

ISSN:0194-911X    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

The effects of high sodium intake (drinking O'9% NaCI for IS days) on the increased renal sympathetic nerve activity and decreased urinary sodium excretion resulting from stressful environmental stimulation (air jet to head) were examined in conscious spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). On a normal sodium intake in SHR, air stress increased renal sympathetic nerve activity 77% and decreased urinary sodium excretion 28% without altering effective renal plasma flow or glomerular filtration rate. By contrast, in conscious SHR on high sodium intake, the same air stress caused a greater increase in renal sympathetic nerve activity (103%) and a greater antinatriuresis (42%) along with reductions in effective renal plasma flow and glomerular filtration rate. Surgical renal denervation prevented the antinatriuretic responses to air stress in other conscious SHR on high or normal sodium intake. In conscious WKY, air stress had no effect on renal sympathetic nerve activity or urinary sodium excretion, regardless of normal or high sodium intake. We conclude that the enhanced renal sympathetic nerve activity and antinatriuretic responses to air stress in conscious SHR on high sodium intake are dependent on a centrally mediated facilitation of sympathetic neural outflow to the kidney. The greater antinatriuretic response to air stress in conscious SHR than in WKY may reflect a greater genetic predisposition in SHR to increase renal sympathetic nerve activity during air stress.

ISSN:0194-911X    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

The purpose of this study was to investigate whether local mechanisms of blood flow autoregulation mediate vasoconstriction during the early development of renal hypertension. Anesthetized rats were instrumented with Doppler flow probes on the celiac (CA), superior mesenteric (SMA), and renal arteries to measure flow velocity in these vessels. Acute two-kidney, one clip renal hypertension was produced by inflating a pneumatic occluder on the left renal artery to reduce flow velocity by 50%. Two hours after renal artery stenosis (RAS), femoral artery pressure (AP) was increased by 35 %, CA resistance by 45 %, and SMA resistance by 57 %. No increases were observed in AP or in CA and SMA resistances for sham-operated, control rats. To determine if autoregulation contributed to the increase in SMA resistance, we protected the SMA vasculature from the increased arterial pressure by servocontrolled inflation of a pneumatic cuff implanted around the SMA. Although normalizing SMA pressure with the protective cuff significantly reduced (p < 0.05) the increase in SMA resistance that occurred after RAS, SMA resistance remained elevated above control levels. These results suggest that (1) reduced intensity of SMA constriction produced by protection of the SMA is due to inhibition of a local autoregulatory mechanism that is contributing to the increase in SMA resistance during the acute development of renal hypertension, and (2) maintenance of elevated SMA resistance during protection from increased AP is the result of pressure-independent mechanisms that are activated subsequent to renal artery stenosis.

ISSN:0194-911X    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

The effects of the calcium entry blocker nitrendipine on blood pressure (BP) and renal hemodynamics were studied in rats with angiotensin II (ANG II) -induced hypertension. The ANG II was infused subcutaneously by implanted osmotic minipumps for 14 to 16 days. There was a progressive rise in BP in ANG H-infused rats to levels 58 mm Hg above basal by Day 10, whereas control rats with sham pumps remained normotensive. Nitrendipine or vehicle was administered by gavage to groups of control and hypertensive rats for 5 days, and clearance experiments were performed with the rats under anesthesia on the last day. The prolonged infusion of ANG II increased the renal vascular resistance and reduced the glomerular filtration rate and renal Na + excretion. At a dose of 3 mg/100 g body weight, nitrendipine had no consistent effects on BP or renal function of control rats. By contrast, in rats with ANG II-induced hypertension, nitrendipine normalized both the BP and the changes in renal vascular resistance and glomerular filtration rate. Despite the fall in BP, nitrendipine caused a marked diuresis and natriuresis. Moreover, nitrendipine increased Na+excretion of conscious, ANG H-hypertensive rats but not of controls. Thus, nitrendipine appears to be highly effective in reversing ANG II-induced hypertension and Na+retention. These findings also indicate that the hypertension, renal vasoconstriction, and Na+retention accompanying prolonged ANG II infusions may be mediated by calcium-dependent mechanisms.

ISSN:0194-911X    

出版商:OVID    

年代:1985

数据来源: OVID