Age-dependent overflow of endogenous norepinephrine from paraventricular hypothalamic nucleus of hypertensive rats

1993 ◽  
Vol 265 (1) ◽  
pp. H39-H46 ◽  
Author(s):  
J. M. Qualy ◽  
T. C. Westfall
Keyword(s):  
Blood Pressure ◽  
Neuronal Activity ◽  
Reciprocal Relationship ◽  
Hypothalamic Nucleus ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Paraventricular Hypothalamic Nucleus ◽  
Wistar Kyoto ◽  
The Relationship

The relationship between age and central noradrenergic neuronal activity of the paraventricular hypothalamic nucleus (PVH) was examined in 7- to 10-, 12- to 14-, and 30- to 36-wk-old Sprague-Dawley (SD), Wistar-Kyoto (WKY), and spontaneously hypertensive rats (SHR). As an index of noradrenergic activity, endogenous norepinephrine (NE) overflow was assessed utilizing a miniaturized push-pull cannula assembly in unanesthetized freely moving rats. NE overlow under basal, 56 mM K+ stimulation, and in response to pressor/depressor drugs, were examined in all three strains at all ages. Significant increases in basal and K(+)-stimulated overflow of endogenous NE from the PVH were observed in all ages of SHR compared with normotensive controls with the greatest percent increase occurring during the development of hypertension in SHR. In addition, a reciprocal relationship exists with respect to blood pressure and overflow of NE from the PVH such that increases/decreases in blood pressure elicit decreases/increases in NE overflow in all strains at all ages examined. However, developing hypertensive SHR exhibited attenuated decreases in overflow of NE from the PVH compared with age-matched controls and established hypertensive SHR. These results suggest that noradrenergic pathways of the PVH contribute to the development and maintenance of arterial pressure hemostasis and that enhanced central noradrenergic neuronal activity is greatest during the development of hypertension in SHR.

Release of norepinephrine from the paraventricular hypothalamic nucleus of hypertensive rats

1988 ◽  
Vol 254 (5) ◽  
pp. H993-H1003 ◽  
Author(s):  
J. M. Qualy ◽  
T. C. Westfall
Keyword(s):  
Blood Pressure ◽  
Age Groups ◽  
Reciprocal Relationship ◽  
Hypothalamic Nucleus ◽  
Sprague Dawley ◽  
Spontaneously Hypertensive ◽  
Paraventricular Hypothalamic Nucleus ◽  
Arterial Blood ◽  
Freely Moving ◽  
Wistar Kyoto

The push-pull cannula was used to examine the release of endogenous norepinephrine (NE) from the paraventricular hypothalamic nucleus (PVH) of unanesthetized freely moving 7- to 10- and 12- to 14-wk-old Sprague-Dawley (SD), Wistar-Kyoto (WKY), and spontaneously hypertensive (SHR) rats. Basal NE release, K+ (56 mM) stimulation-induced NE release, and NE release in response to pressor/depressor drugs were examined in all three strains at both ages. Significant increases in basal and K+-stimulated release of endogenous NE from the PVH were observed in 7- to 10- and 12- to 14-wk-old SHR compared with the normotensive control rats suggesting that enhanced central noradrenergic nerve activity may be involved in the development and maintenance of hypertension in the SHR. In addition, a reciprocal relationship exists with respect to blood pressure and NE release from the PVH, i.e., decreases in blood pressure elicit increases in NE release, and increases in blood pressure elicit decreases in NE release in all three strains at both age groups, suggesting that the noradrenergic pathways of the PVH contribute to the maintenance of arterial blood pressure homeostasis.

The vascular sensitizing character of plasma from spontaneously hypertensive rats

1981 ◽  
Vol 59 (11) ◽  
pp. 1111-1116 ◽  
Author(s):  
Gary L. Wright
Keyword(s):  
Blood Pressure ◽  
Plasma Levels ◽  
Spontaneously Hypertensive Rats ◽  
Vascular Tissue ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Tissue Sensitivity ◽  
Low Levels ◽  
Wistar Kyoto

Experiments were conducted to examine the effects of plasma from spontaneously hypertensive rats (systolic blood pressure (SBP) = 183 torr; 1 torr = 133.322 Pa) on the contractile properties of aortic strips from normotensive rats. While incubated in plasma from spontaneously hypertensive (SH) rats, the aortic strips of normotensive rats exhibited hyperresponsiveness to norepinephrine (NE) compared with those incubated in plasma obtained from Wistar–Kyoto (SBP = 128 torr) or Sprague–Dawley (SBP = 110 torr) rats. The washout of plasma and perfusion of the aortic strips with Krebs bicarbonate solution abolished the effect of SH plasma on the reactivity to NE but not potassium, suggesting a residual hypersensitivity. The comparison of these findings with results obtained for contractions of aortic strips in Krebs bicarbonate solution containing high and low levels of calcium indicated the effect of SH plasma on vascular tissue sensitivity was not directly related to an alteration in plasma levels of calcium.

Heme oxygenase substrates acutely lower blood pressure in hypertensive rats

1996 ◽  
Vol 271 (3) ◽  
pp. H1132-H1138 ◽  
Author(s):  
R. A. Johnson ◽  
M. Lavesa ◽  
K. DeSeyn ◽  
M. J. Scholer ◽  
A. Nasjletti
Keyword(s):  
Blood Pressure ◽  
Carbon Monoxide ◽  
Heme Oxygenase ◽  
Lower Blood Pressure ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Free Iron ◽  
Spontaneously Hypertensive ◽  
Lower Blood ◽  
Wistar Kyoto

Heme oxygenase catalyzes the metabolism of heme to biliverdine, free iron, and carbon monoxide. The current study was designed to determine if treatment with the heme oxygenase substrates heme-L-arginate or heme-L-lysinate, to stimulate formation of heme oxygenase products, can lower blood pressure in the rat. Heme-L-arginate (45 mumol/kg ip) and heme-L-lysinate (45 mumol/kg ip) acutely lowered blood pressure in awake spontaneously hypertensive rats (SHR) by approximately 35 mmHg. For both heme oxygenase substrates, this effect was blunted by pretreatment with an inhibitor of heme oxygenase, zinc deuteroporphyrin 2,4-bis glycol. Heme-L-lysinate also lowered arterial pressure in deoxycorticosterone acetate-salt hypertensive rats and in rats with phenylephrine-induced hypertension, indicating that the vasodepressive actions of heme may be extended to other hypertensive models. However, neither heme-L-arginate nor heme-L-lysinate decreased blood pressure in normotensive controls. The heme oxygenase product biliverdine did not lower blood pressure in SHR, and the vasodepressive actions of heme-L-lysinate were unaffected by pretreatment with deferoxamine to chelate free iron. Carbon monoxide (12 ml/kg ip) lowered blood pressure in SHR and in rats made hypertensive by phenylephrine infusion, had no effect on blood pressure in Wistar-Kyoto rats, and elicited only a modest vasodepressive response in normotensive Sprague-Dawley rats. We conclude that heme-bearing preparations can lower blood pressure in hypertensive rats, presumably via heme oxygenase-mediated formation of carbon monoxide.

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.

Increased Pressor Responsiveness to Enkephalin in Spontaneously Hypertensive Rats: The Role of Vasopressin

1980 ◽  
Vol 59 (s6) ◽  
pp. 235s-237s ◽  
Author(s):  
R. W. Rockhold ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Pressor Response ◽  
Cardiovascular Effects ◽  
Hypertensive Rats ◽  
Methionine Enkephalin ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Wistar Kyoto

1. The cardiovascular effects of an enkephalin analogue were examined in spontaneously hypertensive and normotensive Wistar-Kyoto rats. (D-Ala2)-methionine enkephalin caused a biphasic increase in blood pressure and an increase in heart rate after intracerebroventricular injection. 2. The initial pressor response to (D-Ala2)-methionine enkephalin was greater in hypertensive than in normotensive rats. No difference was noted between groups during the secondary pressor response. Heart rate increases paralleled the secondary increase in blood pressure. 3. Naloxone pretreatment abolished the secondary increase in blood pressure and the tachycardia, but did not blunt the initial pressor response in female Wistar-Kyoto rats. 4. Plasma levels of arginine vasopressin were depressed during the plateau phase of the pressor response in hypertensive rats given intracerebroventricular (d-Ala2)-methionine enkephalin. 5. The results suggest that the cardiovascular effects of central enkephalin are not due to vasopressin, but may involve activation of the sympathetic nervous system.

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

Changes of Blood Pressure Rhythm and Clock Protein Expression Levels in Spontaneously Hypertensive Rats After Ischemia-Reperfusion

2021 ◽  
Author(s):  
Jing Jin ◽  
Yumeng Liu ◽  
Jing Huang ◽  
Dong Zhang ◽  
Jian Ge ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Protein Expression ◽  
Circadian Clock ◽  
Spontaneously Hypertensive Rats ◽  
Ischemia Reperfusion ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Expression Levels ◽  
The Relationship ◽  
Clock Protein

Abstract Objective A variety of circadian patterns of blood pressure after ischemic stroke in patients with essential hypertension appear to be a potential risk of stroke recurrence, but the mechanism is still unclear. This study intends to reveal the changes in blood pressure rhythm and circadian clock protein expression levels in spontaneously hypertensive rats (SHR) after ischemia-reperfusion, and the relationship between the two. Methods Using the SHR middle cerebral artery occlusion experimental model, the systolic blood pressure was continuously monitored for 24 hours after the operation to observe the blood pressure rhythm. The rat tail vein blood was taken every 3h, and the serum CLOCK, BMAL1, PER1 and CRY1 protein expression levels were detected by Elisa. Pearson correlation analysis counted the relationship between SHR blood pressure rhythm and circadian clock protein fluctuation after ischemia-reperfusion. Results The proportion of abnormal blood pressure patterns in the SHR + tMCAO group was significantly higher than that in the SHR group, the serum CLOCK expression was relatively constant, and the circadian rhythm of BMAL1, PER1 and CRY1 protein expression changed significantly. Pearson analysis showed that PER1 protein level was negatively correlated with dipper (r = -0.565, P = 0.002) and extreme-dipper (r = -0.531, P = 0.001) blood pressure, and was significantly positively correlated with non-dipper blood pressure (r = 0.620, P < 0.001). Conclusion The rhythm pattern of blood pressure after ischemia-reperfusion in SHR is obviously disordered, and it is closely related to the regulation of Per1 gene.

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.

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