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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is not known whether high salt diet alters the sarcolemmal Na-K pump activity of resistance vessels in stroke-prone spontaneously hypertensive rats (SHRSP). We examined hindquarters vascular responses to ouabain 10(-3) M in the isolated hindquarters perfused with the Krebs-Henseleit solution in SHRSP and in normotensive Wistar-Kyoto rats (WKY) after two weeks of either normal (0.3% NaCl) or high (8% NaCl) salt diet. Salt loading increased arterial pressure (P less than 0.05) and augmented ouabain-induced vasoconstriction (P less than 0.01) in SHRSP. In WKY, salt loading did not alter arterial pressure or vascular responses to ouabain. Neither hindquarters vascular resistance during maximal vasodilatation produced by nitroprusside nor hindquarters vascular responses to norepinephrine were different between the two groups of SHRSP, which suggested that augmented response to ouabain in SHRSP on high salt diet could not be explained by structural vascular changes. Vasodilatation by phentolamine during maximal vasoconstriction induced by ouabain was also not different between two groups of SHRSP, which suggested that ouabain-induced release of norepinephrine from nerve endings was not different between the two groups of SHRSP. These results suggest that salt loading might augment the sarcolemmal Na-K pump activity of hindquarters resistance vessels in SHRSP but not in WKY. The augmented sarcolemmal Na-K pump activity of resistance vessels may act against salt-induced vasoconstriction in SHRSP.
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PMID:Augmented vascular responses to ouabain in SHRSP during salt loading. 244 10

To investigate the effect of Calcium antagonists (Ca-An) with different tissue specificity in the development of hypertension and stroke in salt-loading SHRSP, three experiments were conducted. In experiment I (1), 50 8-week-old male SHRSP were divided into three groups and given nifedipine (NF, 32 mg/kg/day), menidipine (MN 32 mg/kg/day) and placebo (control group) respectively. In the control group 83.3% (15/18) died of stroke and 17 showed renal vascular sclerosis. Their average lifespan was 84 days. NF and MN significantly reduced systolic blood pressure (SBP), and no stroke of renal vascular sclerosis developed. In experiment I (2), 54 7-week-old male SHRSP were divided into three groups (18 in each group). They were treated with nimodipine (NM) 20 mg/kg/day, 2 mg/kg/day and placebo respectively. NM (20 mg/kg/day) markedly lowered SBP and postponed the onset of stroke. Only 11% died in 17 weeks. NM (2 mg/kg/day did not lower SBP but postpond the onset of stroke. In experiment II (1), 29 10-week-old female SHRSP were divided into three groups: Group A was given NF 32 mg/kg/day, group B was parathyroidectomized (PTX) and group C served as control. PTX group did not lower SBP but could postpone the onset of stroke. In experiment II (2), 33 male SHRSP were divided into three groups and ticated as described above in experiment II (1) (11 in each group). Seven weeks after the experiment, the brain blood flow of NF group was significantly greater (67.5%) than that of the control and PTX groups. In experiment III, 27 7-week-old male SHRSP were divided into three groups as described above in experiment I (2).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium antagonists in prevention of hypertension and stroke in stroke-prone spontaneously hypertensive rats. 250 75

The influence of chronic treatment with the angiotensin I converting enzyme (ACE) inhibitor enalapril on blood pressure, kidney function, and survival was examined in stroke-prone spontaneously hypertensive rats (SHRSP). Male SHRSP that were fed a Japanese rat chow plus a 1% NaCl drinking solution beginning at 7-8 weeks of age developed severe hypertension and stroke; 14 of 18 untreated control SHRSP died by 14 weeks of age and exhibited evidence of cerebrovascular lesions. When enalapril (15 mg/kg/day) was included in the drinking solution of 15 SHRSP, blood pressure was initially reduced by only a slight degree, whereas survival improved markedly; only one of 10 SHRSP died before the rest were killed at 18 to 21 weeks. The remaining five enalapril-treated SHRSP lived beyond 36 weeks and on histological examination exhibited no evidence of cerebrovascular lesions. Chronic enalapril treatment also prevented the greater urinary excretion of protein and severe renal lesions observed in untreated SHRSP but did not affect urinary salt and water excretion. In anesthetized rats, glomerular filtration rate and tubular reabsorption of water were lower in untreated control SHRSP when compared with enalapril-treated SHRSP. Mean arterial pressure was comparable in both groups. These data support a possible role for ACE inhibition in the prevention of stroke and maintenance of kidney function independent of any marked change in blood pressure of SHRSP. Whether the protective effects of ACE inhibition relate to reduced angiotensin II formation, increased tissue kinins, or another mechanism remains to be determined.
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PMID:Enalapril prevents stroke and kidney dysfunction in salt-loaded stroke-prone spontaneously hypertensive rats. 253 41

Smooth muscle relaxation due to activation of Na+-K+-adenosinetriphosphatase (ATPase) (K+ relaxation) was studied in isolated tail arteries from stroke-prone spontaneously hypertensive (SHRSP) and Wistar-Kyoto (WKY) rats. Exposure to K+ (7 mM) relaxed a norepinephrine (1 microM) contraction induced in K+-free physiological salt solution (PSS) by 46 +/- 3% in WKY and by 81 +/- 3% in SHRSP. Incubation with monensin (10 microM) augmented the K+-relaxation in WKY to 61 +/- 5%. Incubation with amiloride (10 microM) or with low-Na+ (10 mM) PSS attenuated the K+ relaxation in SHRSP to 34 +/- 3 and 5 +/- 2%, respectively. Incubation with high-Ca2+ (6.6 mM) PSS attenuated the K+ relaxation in WKY to 25 +/- 3% but resulted in only a slight decrease in the relaxation in SHRSP (to 73 +/- 2%). We conclude 1) that a greater Na+ leakiness of the plasma membrane in SHRSP than in WKY while the Na+ pump is inactive in K+-free PSS can explain the greater relaxation observed when the Na+ pump is reactivated and 2) that the Na+ leakiness of the membrane is more attenuated by Ca2+ in the WKY than in the SHRSP. We hypothesize that this Ca2+ effect reflects a normally large amount of this ion that can be bound to and thereby stabilize the membrane of the WKY, decreasing its permeability to Na+. The membrane of the SHRSP is deficient in its Ca2+-binding sites. Hence the added Ca2+ does not further stabilize its membrane.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Potassium-induced relaxation of arteries in hypertension: modulation by extracellular calcium. 253 82

To explain the pathophysiological significance of endogenous atrial natriuretic polypeptide (ANP) in the development of hypertension, we examined the effect of chronic, repetitive administrations of MAb raised against alpha-rat ANP in two rat models of hypertension, spontaneously hypertensive rats of the stroke prone substrain (SHR-SP), and deoxycorticosterone acetate (DOCA)-salt rats. Weekly intravenous administrations of MAb with high affinity for alpha-rat ANP, named KY-ANP-II (MAb[KY-ANP-II]), started at the age of 6 wk, significantly augmented the rise in blood pressure of SHR-SP, compared with control SHR-SP treated with another MAb with quite low affinity for alpha-rat ANP, named KY-ANP-I (MAb[KY-ANP-I]), throughout the observation period. The administrations of MAb[KY-ANP-II] had no significant effect on blood pressure of age-matched normotensive Wistar Kyoto rats, compared with those receiving MAb[KY-ANP-I]. Weekly administrations of MAb[KY-ANP-II] also significantly aggravated hypertension in DOCA-salt rats. Blood pressure of DOCA-salt rats treated with MAb[KY-ANP-II] was significantly higher than that of DOCA-salt rats treated with MAb[KY-ANP-I] throughout 8 wk of DOCA and 1% saline administration. The administration of MAb[KY-ANP-II] also significantly attenuated exaggerated diuresis and natriuresis in DOCA-salt rats compared with those treated with MAb[KY-ANP-I]. Elevated plasma cGMP levels of both SHR-SP and DOCA-salt rats were significantly reduced by the administration of MAb[KY-ANP-II]. These results suggest the compensatory role of augmented secretion of ANP in these hypertensive rats and support the concept that augmented secretion of ANP could represent an antihypertensive deterrent mechanism.
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PMID:Chronic blockade of endogenous atrial natriuretic polypeptide (ANP) by monoclonal antibody against ANP accelerates the development of hypertension in spontaneously hypertensive and deoxycorticosterone acetate-salt-hypertensive rats. 254 22

The specific competitive alpha 1-postsynaptic blocking action and haemodynamic effects of prazosin (Minipress) have been summarized. Prazosin causes dilatation of arterioles and veins, reduces total peripheral resistance as well as preload and afterload. Cardiac output does not change at rest, stroke volume and subsequent cardiac output increase during exercise. The changes in heart rate have non-significant. It does not cause sympathetic counter-regulation, plasma renin activity does not increase, aldosterone level decreases, salt- and fluid retention may rarely be observed. It does not provoke angina. The authors report on the results of their examinations with the first dose of prazosin in 61 patients (in 33 cases by the double-blind cross-over method by placebo control), and summarize the observations made with the drug in long-term treatment in Hungary. The authors and other teams used prazosin as a long-term treatment (of approximately 3 months) in combination with other drugs in a total of 344 patients, and as monotherapy in 159 patients. In the course of combination treatment side-effects were observed in 15% of the patients (dizziness, headache, weakness, occasionally palpitation). During monotherapy, side-effects occurred in 12% of the patients (tachycardia, headache, weakness, dizziness). Hungarian results confirm the usefulness of prazosin in all stages of hypertension. It is effective in 30-35% of the cases as a monotherapy (this rate is congruent with the efficacy of beta-blockers, calcium antagonists and antihypertensive drugs of central action). Earlier prazosin had been used as a third agent in combination treatment of hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The mechanism of the action of Minipress. Examinations in hypertension. 257 64

The effects of norepinephrine on contractile force development were studied in tail artery strips from spontaneously hypertensive stroke-prone (SHRSP) and Kyoto-Wistar normotensive rats (WKY). The strips were mounted in physiological salt solution between a fixed base and force transducers; isometric contractions were recorded. Norepinephrine-induced were characterized by fluctuations in contractile activity, whereas contractile responses in arteries from WKY remained constant with time. The magnitude and frequency of phasic responses in SHRSP arteries varied directly with increasing concentrations of norepinephrine (1.8 X 10(-9) to 1.8 X 10(-6) M). The phasic responses induced by norepinephrine in SHRSP arteries were reversed by the following experimental interventions: 1) 10(-4) M ouabain; 2) 20 degrees C; 3) potassium-free solution; 4) 1.0 mM BaCl2; 5) 20 mM KCl; 6) 30 mM tetraethylammonium chloride; 7) chloride-free solution; and 8) 10(-7) M D 600 (calcium channel blocker). It is proposed that the phasic contractile responses to norepinephrine in SHRSP are related to altered movements of calcium and potassium across the cell membrane. This study demonstrates a very distinct functional individuality in the arterial vascular smooth muscle cell membrane of SHRSP.
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PMID:Norepinephrine-induced phasic activity in tail arteries from genetically hypertensive rats. 257 88

The sequential effects of an increased daily NaCl intake on hemodynamics, fluid electrolyte balances, and hormonal responses were evaluated in dogs (n = 7) with fixed circulating levels of angiotensin II (ANG II). During the control period, ANG II was infused at 3 ng.kg-1.min-1 while dogs were maintained on an 8 meq NaCl/day diet. Water intake was fixed at 700 ml/day. Continuously recorded (24 h/day) changes of total body weight (TBW) were used as an index of total body water. Cardiac stroke volume and arterial pressure were recorded, and each beat was digitized to provide hourly and 24-h average cardiac output (CO), mean arterial pressure (MAP), and total peripheral resistance (TPR). After three stable control days, daily salt intake was increased to 120 meq for 7 days. TBW increased gradually to 448 +/- 111 g (2.9%, P less than 0.05) above control by day 3. An 11% expansion of blood volume (P less than 0.05) was found (51CR-labeled red blood cells) on day 2 of high NaCl. CO rose 12% and MAP 20% (P less than 0.05) in parallel with TBW by day 4. By day 7, CO remained only 5% elevated, whereas MAP had stabilized at 20% above control levels. TPR remained significantly elevated from days 3 through 7. A positive Na balance averaging 91 +/- 8 meq (P less than 0.05) occurred on day 1. Plasma Na concentration was increased 2-3 meq/l above control throughout the period of high-salt intake. Plasma renin activity and aldosterone levels decreased to nearly undetectable levels, vasopressin rose slightly, and atrial natriuretic peptide levels increased significantly. Dogs maintained at 8 meq/day NaCl during the same infusion of ANG II showed no changes in MAP, CO, TPR, or TBW. In summary, the salt-induced hypertension was consistently related to small but significant fluid retention, blood volume expansion, elevations of cardiac output, and a gradual increase in TPR.
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PMID:Hemodynamics and blood volume in angiotensin II salt-dependent hypertension in dogs. 258 96

Recently, food intake in Japan has been characterized by an increase in fat intake, especially animal-fat intake and the maintenance of excess salt (sodium chloride) intake. It is generally accepted that the increase in fat intake is closely related to atherosclerosis, and excess salt intake is a high risk factor for the development of hypertension and cerebrovascular lesions. So far, in almost all reports, the increase in fat intake and excess salt intake have been studied independently, and there have been few reports on the combined effects of these two factors. Taking the above things into consideration, it would seem to be very interesting to investigate the effect of excess salt intake on lipid metabolism. In this paper, we studied the effects of excess salt intake on lipoprotein and apolipoprotein metabolisms, using stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Kyo: Wistar rats (WKY) as model animals. The results obtained were as follows: A significant increase in the concentration of serum total cholesterol (TC) was observed in SHRSP and WKY, when the rats were given a regular diet (CE-2, Clea Japan Inc.) and 1% sodium chloride solution (1% NaCl) as drinking water for 4 weeks. This was accompanied by a tendency toward increases in the concentrations of serum apolipoproteins in both strains. These results suggest that excess salt intake could accelerate the production of serum total lipoproteins in SHRSP and WKY, when the rats are fed a regular diet. Next, 1% NaCl and a high-fat and high-cholesterol diet (HFC diet) were simultaneously given to SHRSP and WKY for 6 weeks. The effects of simultaneous administration on lipoprotein and apolipoprotein metabolisms were compared with those of HFC feeding. One percent NaCl did not markedly affect hypercholesterolemia in WKY, while it induced more marked hypercholesterolemia in SHRSP that was associated with extreme elevations of serum TC and the atherogenic index (A.I.). This deleterious effect of 1% NaCl in SHRSP was due to drastic elevations of cholesterol contents in the very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL) and low density lipoprotein (LDL) fractions. This was also associated with marked increases in apo B contents in the VLDL, IDL and LDL fractions and significant increases in apo E contents in the VLDL and IDL fractions. These results indicate that 1% NaCl induced much larger increases in serum atherogenic beta-lipoproteins in SHRSP.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Studies on stroke-prone spontaneously hypertensive rats (SHRSP) fed a high-fat and high-cholesterol diet--effects of salt intake on serum lipoprotein and apolipoprotein metabolism]. 263 85

Hypernatremia is a potentially life-threatening electrolyte abnormality. This problem develops most often because of loss of water from the animal, but in rare cases hypernatremia results from gain of sodium chloride. Important conditions predisposing to hypernatremia include diarrhea, vomiting, heat stroke, fever, limited access to water, excessive diuretic use, renal diseases, and pituitary diabetes insipidus. This condition rarely develops if animals have adequate access to water. Clinical signs relate to central nervous system derangements and can progress to seizures and coma. Diagnosis is based on the serum sodium concentration; treatment should be instituted if it is greater than 170 mEq per L. Treatment is based on knowledge of the volume status of the patient and the probable cause for the hypernatremia. In general, 5 per cent dextrose in water or other hypotonic fluids are given slowly intravenously. The rate of administration should be adjusted so the water deficit is replaced over 48 to 72 h. Too rapid correction of hypernatremia can lead to cerebral edema and worsening of the animal. In cases of salt intoxication, diuretics must be given in addition to slow water replacement to avoid the development of pulmonary edema.
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PMID:Hypernatremia. 264 64


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