scholarly journals Role of NO on pressure-natriuresis in Wistar-Kyoto and spontaneously hypertensive rats

1993 ◽  
Vol 43 (1) ◽  
pp. 205-211 ◽  
Author(s):  
Hideki Ikenaga ◽  
Hiromichi Suzuki ◽  
Naohito Ishii ◽  
Hajime Itoh ◽  
Takao Saruta
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Pressure Natriuresis

Norepinephrine levels in paraventricular nucleus of spontaneously hypertensive rats: role of neuropeptide Y

1993 ◽  
Vol 265 (3) ◽  
pp. H893-H898 ◽  
Author(s):  
N. D. Woo ◽  
K. Mukherjee ◽  
P. K. Ganguly
Keyword(s):  
Neuropeptide Y ◽  
Paraventricular Nucleus ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Central Neurons ◽  
Sympathetic Regulation ◽  
Series Of Experiments ◽  
Wistar Kyoto

Recent evidence supports the view that the sympathetic system actively participates in the development of hypertension. Because norepinephrine, contained within central neurons involved in cardiovascular sympathetic regulation, is known to coexist with neuropeptide Y, it is possible that a functional interaction between neuropeptide Y and norepinephrine exists within the brain. In an effort to clarify whether or not central catecholamine systems are modulated by neuropeptide Y in hypertensive situations, the paraventricular nucleus of spontaneously hypertensive rats was exposed to neuropeptide Y (10(-9) M), and levels of norepinephrine were sampled by microdialysis. Norepinephrine levels in spontaneously hypertensive rats were significantly increased and did not change after exposure to neuropeptide Y, in sharp contrast to the decreases seen in Wistar-Kyoto controls. To ascertain whether these alterations in norepinephrine control were specific to the model used, a similar series of experiments was carried out in the paraventricular nucleus of aortic-banded rats. These studies supported the previous findings. Norepinephrine levels in aortic-banded rats were markedly elevated when compared with sham-operated controls and demonstrated no change after exposure to neuropeptide Y, whereas decreases of > 50% were seen in sham-operated controls. These results support the view that mechanisms normally involving neuropeptide Y as a neuromodulator in the paraventricular nucleus are altered in hypertensive situations. It is suggested that hypertension may precipitate changes in mechanisms involving brain neuropeptide Y and increased sympathetic activity.

scholarly journals Role of cholinergic receptors in adrenal catecholamine secretion in spontaneously hypertensive rats

1999 ◽  
Vol 277 (4) ◽  
pp. R1057-R1062 ◽  
Author(s):  
Takahiro Nagayama ◽  
Takayuki Matsumoto ◽  
Makoto Yoshida ◽  
Mizue Suzuki-Kusaba ◽  
Hiroaki Hisa ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Muscarinic Receptors ◽  
Nicotinic Receptors ◽  
Spontaneously Hypertensive Rats ◽  
Adrenal Glands ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Wistar Kyoto

We investigated the role of nicotinic and muscarinic receptors in secretion of catecholamines induced by transmural electrical stimulation (ES) from isolated perfused adrenal glands of spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto (WKY) rats. ES (1–10 Hz) produced frequency-dependent increases in epinephrine (Epi) and norepinephrine (NE) output as measured in perfusate. The ES-induced increases in NE output, but not Epi output, were significantly greater in adrenal glands of SHRs than in those of WKY rats. Hexamethonium (10–100 μM) markedly inhibited the ES-induced increases in Epi and NE output from adrenal glands of SHRs and WKY rats. Atropine (0.3–3 μM) inhibited the ES-induced increases in Epi and NE output from adrenal glands of SHRs, but not from those of WKY rats. These results suggest that endogenous acetylcholine-induced secretion of adrenal catecholamines is predominantly mediated by nicotinic receptors in SHRs and WKY rats and that the contribution of muscarinic receptors may be different between these two strains.

Renal interstitial hydrostatic pressure during pressure natriuresis in hypertension

1988 ◽  
Vol 255 (5) ◽  
pp. R756-R759 ◽  
Author(s):  
A. A. Khraibi ◽  
F. G. Knox
Keyword(s):  
Hydrostatic Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Left Kidney ◽  
Hypertensive Rats ◽  
Polyethylene Matrix ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Fractional Excretion Of Sodium ◽  
Wistar Kyoto ◽  
Pressure Natriuresis

The objective of this study was to test the hypothesis that changes in renal perfusion pressure (RPP) are not fully transmitted to the renal interstitium in spontaneous hypertension in comparison with normotensive states. Okamoto spontaneously hypertensive and normotensive Wistar-Kyoto rats were used in this study. Renal interstitial hydrostatic pressure (RIHP) was measured directly and continuously via a polyethylene matrix that was implanted chronically in the left kidney 3 wk before RIHP measurement. When RPP was allowed to increase from 136 +/- 0.5 to 162 +/- 1.3 mmHg in male spontaneously hypertensive rats, RIHP was not significantly changed from 3.7 +/- 0.9 to 4.6 +/- 1.1 mmHg, and fractional excretion of sodium (FENa) increased significantly from 0.26 +/- 0.12 to 0.65 +/- 0.15% (P less than 0.05). When RPP was allowed to change from 104 +/- 0.9 to 127 +/- 1.3 mmHg in male Wistar-Kyoto rats, RIHP increased markedly from 4.0 +/- 0.3 to 7.2 +/- 0.4 mmHg (P less than 0.05), and FENa was significantly elevated from 0.27 +/- 0.08 to 2.02 +/- 0.55% (P less than 0.05). In conclusion, spontaneously hypertensive rats have a blunted increase in RIHP and pressure natriuresis response in comparison with Wistar-Kyoto rats. Thus, in Okamoto spontaneously hypertensive rats, the effect of RPP on RIHP is attenuated, leading to a blunted pressure natriuresis response.

Role of endogenous centrally released NO in cardiovascular adaptation to hypovolemia in WKY and SHR

1997 ◽  
Vol 272 (5) ◽  
pp. H2282-H2288 ◽  
Author(s):  
P. Paczwa ◽  
A. S. Budzikowski ◽  
E. Szczepanska-Sadowska
Keyword(s):  
Heart Rate ◽  
Spontaneously Hypertensive Rats ◽  
Hypotensive Effect ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Time Control ◽  
Artificial Cerebrospinal Fluid ◽  
In Series ◽  
Wistar Kyoto

The role of endogenous centrally released nitric oxide (NO) during hypovolemia was investigated in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Bleeding of the rats (1.3% of blood volume) was performed after intracerebroventricular (ICV) administration of: 1) artificial cerebrospinal fluid (series 1, time control, 8 WKY and 8 SHR); 2) 0.5 mg NG-nitro-L-arginine (L-NNA, 2.3 nmol), an inhibitor of NO synthesis (series 2, 8 WKY and 7 SHR); and 3) 0.5 mg L-NNA followed by 1 mg (5.8 nmol) of L-arginine (L-Arg) (6 WKY and 5 SHR). In WKY, hypotension was associated with significant bradycardia (P < 0.001), whereas in SHR slight acceleration of heart rate was observed. In series 2 hemorrhage resulted in a small but significant increase of mean arterial pressure (MAP; P < 0.05) and considerable tachycardia (P < 0.001). In SHR, L-NNA did not modify the decrease of MAP during hypovolomia, and bleeding resulted in a significant bradycardia (P < 0.001). Pretreatment with L-Arg in series 3 was able to reverse the effects of L-NNA on changes of MAP and heart rate during hypovolemia. The results indicate that the central nitroxidergic system plays a significant role in eliciting hypotension and bradycardia in normotensive WKY during hemorrhage. Function of the central nitroxidergic system is significantly altered in SHR in which NO appears to prevent hemorrhagic bradycardia and to reduce the hypotensive effect.

Chronic exercise decreases adrenergic agonist-induced vasoconstriction in spontaneously hypertensive rats

1996 ◽  
Vol 271 (3) ◽  
pp. H977-H983 ◽  
Author(s):  
H. I. Chen ◽  
I. P. Chiang
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Carotid Arteries ◽  
Peak Oxygen Consumption ◽  
Chronic Exercise ◽  
Hypertensive Rats ◽  
Adrenergic Agonist ◽  
Spontaneously Hypertensive ◽  
Effective Training ◽  
Wistar Kyoto

This study was conducted to investigate the effects of chronic exercise on adrenergic agonist-induced vascular responses in spontaneously hypertensive rats (SHR). Four-week-old male SHR and Wistar-Kyoto rats were divided into control and trained groups. The trained groups ran on a drum exerciser at 70% of peak oxygen consumption for 60 min/day 5 days/wk for 10 wk. Resting systolic blood pressure and heart rate were measured by a tail-cuff method, and changes in these parameters were considered as indexes of effective training. At the end of experiments, thoracic aortas and carotid arteries were isolated. Vasoconstricting responses to norepinephrine (NE) or phenylephrine (PHE) were studied. To clarify the role of endothelium-derived nitric oxide (EDNO) in the alteration of NE-induced vasoconstriction after chronic exercise, we measured the changes in vasoconstricting responses to NE (10(-8) M) after treatment with N omega-nitro-L-arginine. Vasorelaxing responses to PHE or clonidine were also studied. Our results showed that 1) vasoconstricting responses to NE or PHE in the endothelium-intact thoracic aorta were reduced, whereas PHE- or clonidine-induced EDNO release was enhanced by exercise training, and 2) the latter could be eliminated by N omega-nitro-L-arginine. Therefore, training may decrease adrenergic agent-induced vasoconstricting responses by increasing their stimulated EDNO release in hypertensive and normotensive rats.

Plasma parathyroid hormone during the development of spontaneous hypertension in rats

1987 ◽  
Vol 65 (12) ◽  
pp. 2386-2389 ◽  
Author(s):  
P. K. T. Pang ◽  
S. Harvey ◽  
P. A. Doris
Keyword(s):  
Parathyroid Hormone ◽  
Spontaneously Hypertensive Rats ◽  
Spontaneous Hypertension ◽  
Hypertensive Rats ◽  
Intact Pth ◽  
Spontaneously Hypertensive ◽  
Blood Pressures ◽  
Wistar Kyoto ◽  
Tail Cuff

Plasma parathyroid hormone levels (pPTH) have been measured by radioimmunoassay (RIA) in young spontaneously hypertensive rats (SHR) and normotensive Wistar–Kyoto controls (WKY) aged from 6 to 16 weeks to assess the possible role of PTH during the development of hypertension. Three antisera were used in the RIAs. One antiserum was directed toward the inactive C-terminal fragment of PTH, another toward the bioactive N-terrninal fragment (PTH 1–34), and a third was obtained by immunization against intact PTH 1–84. Blood pressures were measured by tail-cuff plethysmography with prewarming. Blood ionized calcium and sodium concentrations (b[Ca2+] and b[Na+]) were determined by ion-selective electrolyte analysis. No significant differences were observed between pPTH in the SHR compared with WKY during the development of hypertension. Neither were significant differences in b[Ca2+] or b[Na+] present at any age. The expected progression of hypertension in SHRs was observed and blood pressure was significantly greater in SHR than in WKY at all times. The results suggest that differences in pPTH and b[Ca2+] in SHR reported in other studies may be secondary phenomena to the establishment of hypertension. Our data suggest that PTH is not involved in the pathogenetic processes occurring during the development of spontaneous hypertension in rats.

Impairment of endothelium-dependent dilatation of basilar artery during chronic hypertension

1990 ◽  
Vol 259 (5) ◽  
pp. H1455-H1462 ◽  
Author(s):  
W. G. Mayhan
Keyword(s):  
Nitric Oxide ◽  
Basilar Artery ◽  
Intravital Microscopy ◽  
Spontaneously Hypertensive Rats ◽  
Chronic Hypertension ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Baseline Diameter

The goal of this study was to determine whether responses of the basilar artery are altered during chronic hypertension. We measured the diameter of the basilar artery using intravital microscopy in normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). Acetylcholine (10 microM) dilated the basilar artery by 25 +/- 4% (means +/- SE) in WKY but by only 2 +/- 2% in SHR. Bradykinin (1.0 microM) dilated the basilar artery by 12 +/- 1% in WKY, but did not alter diameter in SHR (-0.1 +/- 2%). In contrast, nitroglycerin produced similar vasodilatation in WKY and SHR. Next, we examined the possibility that impaired vasodilatation in SHR may be related to the production of a cyclooxygenase constrictor substance. Indomethacin (10 mg/kg iv) did not restore vasodilatation in response to acetylcholine and bradykinin in SHR. Finally, we examined the role of nitric oxide in dilatation of the basilar artery in response to acetylcholine and bradykinin in WKY. NG-Monomethyl-L-arginine (L-NMMA; 1.0 microM) had little effect on baseline diameter but inhibited vasodilation in response to acetylcholine and bradykinin. Vasodilatation in response to nitroglycerin was not altered by L-NMMA. These findings suggest a profound impairment of endothelium-dependent dilatation of the basilar artery during chronic hypertension. In addition, impaired vasodilatation is not related to the production of a cyclooxygenase constrictor substance. Furthermore, dilatation of the basilar artery in WKY in response to acetylcholine and bradykinin appears to be related to the production of nitric oxide or a substance capable of liberating nitric oxide.

Role of renal nerves on pressure natriuresis in spontaneously hypertensive rats

1991 ◽  
Vol 260 (1) ◽  
pp. F81-F85 ◽  
Author(s):  
M. Yoshida ◽  
S. Satoh
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Renal Denervation ◽  
Plasma Renin ◽  
Renal Nerves ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Rightward Shift ◽  
Fractional Excretion Of Sodium ◽  
Wistar Kyoto ◽  
Pressure Natriuresis

An abnormal rightward shift of the pressure-natriuresis curve is a well known feature of the renal function in hypertension. The participation of intrinsic neural factors in the kidney in this phenomenon was investigated in anesthetized young and adult spontaneously hypertensive rats (SHR). At 7-8 wk of age, the renal pressure-diuresis curve and pressure-natriuresis curve were shifted to the left in denervated SHR compared with innervated animals. Fractional excretion of sodium was higher, and plasma renin activity was lower in denervated SHR. Glomerular filtration rate was not affected by renal denervation. In 13- to 15-wk-old SHR, renal denervation did not affect the pressure-diuresis and -natriuresis curves, although other parameters were changed compared with the results at 7-8 wk. In Wistar-Kyoto rats, the pressure-diuresis curve was shifted to the left by renal denervation at both ages. These results suggest that the renal nerves have an important effect on the renal pressure-diuresis and -natriuresis curves. However, renal innervation cannot be thought to cause an abnormal rightward shift of the pressure-diuresis and -natriuresis curves in SHR, especially in the established stage of hypertension.

Sign in / Sign up

Export Citation Format

Share Document