Dietary Na and baroreflex modulation of blood pressure and RSNA in normotensive vs. spontaneously hypertensive rats

1994 ◽  
Vol 266 (2) ◽  
pp. H496-H502 ◽  
Author(s):  
B. S. Huang ◽  
F. H. Leenen
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Sodium Intake ◽  
Marked Change ◽  
Dietary Sodium ◽  
Hypertensive Rats ◽  
Baroreflex Control ◽  
Spontaneously Hypertensive ◽  
High Sodium ◽  
Wistar Kyoto

Different changes in baroreflex control of the circulation have been postulated to play a role in the different blood pressure (BP) effects of dietary sodium in normotensive vs. genetically hypertensive rats. We therefore evaluated in young Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR), with or without chronic sinoaortic denervation (SAD), the effects of low, regular, and high dietary sodium intake from 4 to 8 wk of age on BP and baroreflex function. The latter was assessed by changes in renal sympathetic nerve activity (RSNA) and heart rate in response to (de)pressor agents. In SHR, the above range of sodium caused a marked change in resting BP, somewhat more in intact (48 mmHg) vs. SAD (36 mmHg) rats. In contrast, in WKY this range of sodium intake caused only a minor (7 mmHg) change in resting BP of intact WKY but a significant (16 mmHg) change in WKY with SAD, mainly due to an increase in BP on high sodium. In intact WKY increasing dietary sodium from low to regular to high caused stepwise increases in the gain of the RSNA-BP reflex, whereas in intact SHR only an increase from low to regular sodium intake increased the gain. After SAD, the gain of the RSNA-BP reflex was very low, and no longer affected by dietary sodium in either strain. These data suggest that in WKY a sensitization in arterial baroreflex control of RSNA prevents a sodium-induced increase in BP.(ABSTRACT TRUNCATED AT 250 WORDS)

Prevention of hypertension and maintenance of normotension in spontaneously hypertensive rats is dependent on continuous severe dietary sodium restriction

1987 ◽  
Vol 65 (4) ◽  
pp. 573-578 ◽  
Author(s):  
Esther A. Wilczynski ◽  
Frans H. H. Leenen
Keyword(s):  
Blood Pressure ◽  
Sympathetic Activity ◽  
Spontaneously Hypertensive Rats ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Ganglionic Blockade ◽  
Dietary Sodium Restriction

Spontaneously hypertensive rats were placed on a very low (9 μmol/g) or control (101 μmol/g) sodium diet at birth or 4 weeks of age. These diets were continued to 16 weeks of age, or at 10 weeks were increased from 9 to 26 or 101 μmol/g. Sodium restriction initiated up to 4 weeks of age and continued to 16 weeks of age severely retarded growth, prevented the development of hypertension, and reduced effective sympathetic activity as assessed by the response of blood pressure to ganglionic blockade. Only a small increase in sodium intake at 10 weeks of age (to 26 μmol/g or more) resulted in a marked increase in growth rate, an elevation of blood pressure, and a return of the response to ganglionic blockade towards normal. These data indicate that very severe sodium restriction must be continuous to maintain decreased sympathetic activity and normal blood pressure in spontaneously hypertensive rats. It appears that severe dietary sodium restriction suppresses one or more of the mechanisms involved in normal growth and development of hypertension in spontaneously hypertensive rats, but these mechanisms may still proceed once the sodium intake is increased.

Dietary sodium restriction and blood pressure response to sympathetic blockade in young versus adolescent spontaneously hypertensive rats

1990 ◽  
Vol 68 (1) ◽  
pp. 46-50 ◽  
Author(s):  
Frans H. H. Leenen ◽  
Giannoula Klement
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Sodium Intake ◽  
Blood Pressure Response ◽  
Dietary Sodium ◽  
Sympathetic Blockade ◽  
Sodium Restriction ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Dietary Sodium Restriction

The effects of dietary sodium restriction on the maintenance of blood pressure (BP) by sympathetic tone were evaluated in young versus more mature spontaneously hypertensive rats (SHR) and Wistar–Kyoto rats (WKY). Sympathetic activity was assessed by BP responses to α1-receptor blockade (prazosin), central inhibition of sympathetic outflow (clonidine), and by ganglionic blockade (hexamethonium). On regular sodium intake, SHR showed elevated BP and increased BP responses to sympathetic blockade at both 10 and 16 weeks of age. Sodium restriction to 9 or 17 μmol Na+/g food prevented or blunted development of hypertension in SHR when started at 4 weeks of age but did not affect BP when started at 10 weeks of age. Sodium restriction initiated in young SHR also prevented development of increased BP responses to sympathetic blockade. However, sodium restriction in more mature SHR did not decrease the increased BP responses to sympathetic blockade. We conclude that prevention of development of sympathetic hyperactivity in young SHR represents a major mechanism in the antihypertensive effect of sodium restriction in young SHR.Key words: dietary sodium, blood pressure, spontaneously hypertensive rats, age, sympathetic blockade.

Effects of dietary Ca2+ on erythrocyte Na+-transport systems in spontaneously hypertensive rats

1991 ◽  
Vol 81 (1) ◽  
pp. 107-112 ◽  
Author(s):  
K. Fujito ◽  
M. Yokomatsu ◽  
N. Ishiguro ◽  
H. Numahata ◽  
Y. Tomino ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Transport Systems ◽  
Hypertensive Rats ◽  
Na Transport ◽  
Spontaneously Hypertensive ◽  
Na Pump ◽  
Wistar Kyoto ◽  
Increased Activity ◽  
Regulation Of Blood Pressure

1. The purpose of this study was to determine the effect of dietary Ca2+ intake on blood pressure and erythrocyte Na+ transport in spontaneously hypertensive rats. 2. Spontaneously hypertensive rats and Wistar-Kyoto rats were fed diets with three different Ca2+ contents, 0.1% (low-Ca2+ diet), 0.6% (normal-Ca2+ diet) and 4.0% (high-Ca2+ diet), between 6 and 20 weeks of age. At 20 weeks of age, the levels of erythrocyte Na+ efflux, as well as Na+ and K+ contents in erythrocytes, were measured. 3. On the low-Ca2+ diet, spontaneously hypertensive rats showed an enhancement of hypertension. Conversely, on the high-Ca2+ diet, they showed an attenuation of the increase in blood pressure. Spontaneously hypertensive rats had a lower erythrocyte Na+ content and increased activity of the Na+ pump at higher levels of dietary Ca2+. Passive Na+ permeability and Na+-K+ co-transport were similar in spontaneously hypertensive rats on the low-, normal- and high-Ca2+ diets. There were no significant differences in blood pressure and in Na+ pump activity in WKY on the three different diets. 4. It is concluded that dietary Ca2+ might affect the regulation of blood pressure in spontaneously hypertensive rats by changing the activity of Na+ pump in the cell membrane.

Metformin decreases plasma insulin levels and systolic blood pressure in spontaneously hypertensive rats

1994 ◽  
Vol 267 (4) ◽  
pp. H1250-H1253 ◽  
Author(s):  
S. Verma ◽  
S. Bhanot ◽  
J. H. McNeill
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Plasma Insulin ◽  
Metformin Treatment ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Insulin Levels ◽  
Plasma Insulin Levels ◽  
Wistar Kyoto

To determine the relationship between hyperinsulinemia and hypertension in spontaneously hypertensive rats (SHR), the antihyperglycemic agent metformin was administered to SHR and their Wistar-Kyoto (WKY) controls, and its effects on plasma insulin levels and blood pressure were examined. Five-week-old rats were started on oral metformin treatment (350 mg.kg-1.day-1, which was gradually increased to 500 mg.kg-1.day-1 over a 2-wk period). Metformin treatment caused sustained decreases in plasma insulin levels in the SHR (27.1 +/- 2.3 vs. untreated SHR 53.5 +/- 2.7 microU/ml, P < 0.001) without having any effect in the WKY (30.7 +/- 2.2 vs. untreated WKY 37.8 +/- 1.6 microU/ml, P > 0.05). The treatment did not affect the plasma glucose levels in any group. Metformin treatment also attenuated the increase in systolic blood pressure in the SHR (157 +/- 6.0 vs. untreated SHR 196 +/- 9.0 mmHg, P < 0.001) but had no effect in the WKY (134 +/- 3 vs. untreated WKY 136 +/- 4 mmHg, P > 0.05). Furthermore, raising plasma insulin levels in the metformin-treated SHR to levels that existed in the untreated SHR reversed the effect of metformin on blood pressure (189 +/- 3 vs. untreated SHR 208 +/- 5.0 mmHg, P > 0.05). These findings suggest that either hyperinsulinemia may contribute toward the increase in blood pressure in the SHR or that the underlying mechanism is closely associated with the expression of both these disorders.

Contribution of Vascular Nitric Oxide to Basal Blood Pressure in Conscious Spontaneously Hypertensive Rats and Normotensive Wistar Kyoto Rats

1995 ◽  
Vol 89 (2) ◽  
pp. 177-182 ◽  
Author(s):  
Naoyoshi Minami ◽  
Yutaka Imai ◽  
Jun-Ichiro Hashimoto ◽  
Keishi Abe
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Methyl Ester ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Basal Blood Pressure ◽  
Wistar Kyoto

1. The aim of this study was to clarify the extent to which vascular nitric oxide contributes to basal blood pressure in conscious spontaneously hypertensive rats and normotensive Wistar Kyoto rats. 2. The contribution of vascular nitric oxide to maintenance of blood pressure was estimated by measuring the pressor response to an intravenous injection of nitric oxide synthase inhibitor, Nω-l-arginine methyl ester, given after serial injections of captopril, vasopressin V1-receptor antagonist (V1-antagonist) and ganglion blocker (pentolinium) in conscious spontaneously hypertensive and Wistar Kyoto rats aged 20–28 weeks. To estimate the ‘amplifier property’ of hypertrophied vasculature in spontaneously hypertensive rats, which is known to modulate pressor responses, the lower blood pressure plateau after serial injections of captopril, V1-antagonist and pentolinium and the maximum blood pressure elicited by subsequent injection of increasing doses of phenylephrine were also measured. 3. The serial injections of captopril, V1-antagonist and pentolinium decreased mean arterial pressure from 164 ± 9 mmHg to 67 ± 2 mmHg and from 117 ± 2 mmHg to 49 ± 1 mmHg in spontaneously hypertensive and Wistar Kyoto rats respectively. The subsequent injection of Nω-l-arginine methyl ester restored mean arterial pressure almost to its control levels in both spontaneously hypertensive and Wistar Kyoto rats. The absolute changes in mean arterial pressure elicited by Nω-l-arginine methyl ester were significantly greater in spontaneously hypertensive than in Wistar Kyoto rats (P < 0.01), but there was no significant difference in the responses to Nω-l-arginine methyl ester when they were expressed as percentages of either the lower blood pressure plateau or maximum blood pressure. 4. These results indicate that basal blood pressure in both spontaneous hypertensive and Wistar Kyoto rats is maintained by a balance between vascular nitric oxide and major pressor systems. They also suggest that the vasodilatory effect of vascular nitric oxide does not differ between spontaneously hypertensive and Wistar Kyoto rats, and that the increased pressor effect of Nω-l-arginine methyl ester in spontaneously hypertensive rats is due to a vascular amplifier mechanism.

Ca2+ sensitization and Ca2+ entry in the control of blood pressure and adrenergic vasoconstriction in conscious Wistar–Kyoto and spontaneously hypertensive rats

2013 ◽  
Vol 31 (10) ◽  
pp. 2025-2035 ◽  
Author(s):  
Michal Behuliak ◽  
Mária Pintérová ◽  
Michal Bencze ◽  
Miriam Petrová ◽  
Silvia Líšková ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

Hypertension transmitted by kidneys from stroke-prone spontaneously hypertensive rats

1989 ◽  
Vol 257 (2) ◽  
pp. F197-F203 ◽  
Author(s):  
R. Rettig ◽  
H. Stauss ◽  
C. Folberth ◽  
D. Ganten ◽  
B. Waldherr ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Transplantation ◽  
Spontaneously Hypertensive Rats ◽  
Plasma Renin ◽  
F1 Hybrids ◽  
Hypertensive Rats ◽  
Plasma Urea ◽  
Spontaneously Hypertensive ◽  
Major Function ◽  
Wistar Kyoto

We determined whether transplantations of kidneys from stroke-prone spontaneously hypertensive rats (SPSHR) and from normotensive Wistar-Kyoto rats (WKY) alter blood pressure in renal graft recipients. Kidneys taken from seven male SPSHR and seven male WKY rats (blood pressure 186 +/- 4.8 and 111 +/- 3.7 mmHg, respectively) at the age of 20 wk were transplanted, using microsurgical techniques, to bilaterally nephrectomized age-matched male F1 hybrids (blood pressure 136 +/- 2.6 and 138 +/- 6.3 mmHg, respectively) bred from SPSHR and WKY parents. After renal transplantation, blood pressure in recipients of SPSHR kidneys rose to 146 +/- 11.8 (week 2), 163 +/- 16.4 (week 3), 192 +/- 17.1 (week 4), 222 +/- 17.7 (week 5), 221 +/- 12.6 (week 6), 218 +/- 20.3 (week 7), and 239 +/- 9.2 mmHg (week 8). There was no significant change in blood pressure in recipients of WKY kidneys. All rats recovered rapidly from surgery. After renal transplantation, there was a significant increase in daily water intake, a decrease in plasma renin activity, and a slight rise in plasma urea concentration. Our data show that transplantation of kidneys from adult SPSHR causes hypertension in normotensive recipients, indicating a major function for the kidney in SPSHR hypertension.

scholarly journals Duration of Electrically Induced Atrial Fibrillation Is Augmented by High Voltage of Stimulus with Higher Blood Pressure in Hypertensive Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Tomomi Nagayama ◽  
Yoshitaka Hirooka ◽  
Akiko Chishaki ◽  
Masao Takemoto ◽  
Yasushi Mukai ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Blood Pressure ◽  
Arterial Pressure ◽  
High Voltage ◽  
Spontaneously Hypertensive Rats ◽  
Low Voltage ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
High Stimulus ◽  
Wistar Kyoto

Objective.Many previous clinical studies have suggested that atrial fibrillation (AF) is closely associated with hypertension. However, the benefits of antihypertensive therapy on AF are still inconsistent, and it is necessary to explore the factors augmenting AF in hypertensive rats. The aim of the present study was to investigate the correlation between arterial pressure or voltage stimulus and to the duration of electrically induced AF in normotensive or hypertensive rats.Methods.AF was reproducibly induced by transesophageal atrial burst pacing in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). We did the burst pacing at high (20 V) or low (5 V) voltage.Results.Duration of AF did not correlate with systolic blood pressure (SBP) and stimulus voltage in WKY. However, only in SHR, duration of AF with high stimulus voltage significantly correlated with SBP and was significantly longer in high than in low voltage stimulus.Discussion and Conclusion.Duration of AF is augmented by high voltage stimulus with higher blood pressure in SHR.

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