The correlation of cardiac mass with arterial haemodynamics of resistive and capacitive load in rats with normotension and established hypertension

American Journal of Physiology-Heart and Circulatory Physiology

1997

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Chen, Hsing I., and Cheng Tao Hu. Endogenous nitric oxide on arterial hemodynamics: a comparison between normotensive and hypertensive rats. Am. J. Physiol. 273 (Heart Circ. Physiol. 42): H1816-H1823, 1997.-Endogenous nitric oxide (NO) plays an important role in maintaining a vasodilator tone. In the present study, we compared the effects of NO blockade on the steady and pulsatile components of arterial hemodynamics between spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto strain (WKY), 22-26 wk of age. In the first series of experiments, various doses (1-30 mg/kg iv) of N G -nitro-L-arginine methyl ester (L-NAME) were administered to block the NO release in anesthetized WKY and SHR. In both WKY and SHR, L-NAME caused a dose-dependent increase in arterial pressure (AP) with a decrease in heart rate (HR). The maximal effects of L-NAME on AP and HR occurred at a dose of 10 mg/kg. Both the AP increase and HR decrease were higher in SHR (AP, ϩ38 Ϯ 4 mmHg; HR, Ϫ49 Ϯ 5 beats/min) than WKY (AP, ϩ22 Ϯ 3 mmHg; HR, Ϫ33 Ϯ 5 beat/min). In other series, the technique of impedance spectral analysis was employed to investigate the effects of L-NAME (10 mg/kg iv) on the arterial hemodynamics. The aortic pressure and flow waves were recorded and subjected to Fourier transform for the analysis of impedance spectra. Both in WKY (n ϭ 12) and in SHR (n ϭ 12), L-NAME significantly increased AP and total peripheral resistance (TPR). The pulsatile and frequency-dependent hemodynamics including characteristic impedance, wave reflection, and ventricular work were only slightly altered. Despite higher resting values of AP and TPR in SHR (mean AP, 154 Ϯ 7 mmHg; mean TPR, 204 Ϯ 17 ϫ 10 3 dyn·s·cm Ϫ5 ) than WKY (mean AP, 94 Ϯ 6 mmHg; mean TPR, 98 Ϯ 12 ϫ 10 3 dyn·s·cm Ϫ5 ), the magnitudes of AP and TPR increments after NO blockade were significantly higher in SHR (AP, ϩ37 Ϯ 3 mmHg; TPR, ϩ124 Ϯ 16 ϫ 10 3 dyn·s·cm Ϫ5 ) than in WKY (AP, ϩ24 Ϯ 3 mmHg; TPR, ϩ45 Ϯ 7 ϫ 10 3 dyn·s·cm Ϫ5 ). The continuous formation of endogenous NO affects predominantly the AP and peripheral resistance in both WKY and SHR. The windkessel functions, such as impedance spectra, pulse-wave reflection, and ventricular work, are less affected after NO blockade. In addition, the effects of NO release on the AP and TPR appear to be enhanced in rats with established hypertension.Fourier analysis; arterial impedance IT HAS BEEN WELL DOCUMENTED that continuous release of endogenous nitric oxide (NO) maintains a dilator tone in the vascular tissues (27,28). In isolated aortic rings (10,14,32,37) and perfused vascular beds (1,18,39,40), NO blockade with N G -monomethyl-L-arginine (L-NMMA) or N G -nitro-L-arginine methyl ester (L-NAME) inevitably caused vasoconstriction. In the whole body, blockade of NO release significantly caused an increase in systemic arterial pressure (AP) (34, 36). The increase in AP was accompanied by an increase in vascular resistance and a decrease in blood flow in various vascular beds (7-9). There is little doubt that endothelium-deriv...

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confidence: 99%

Section: H1819 No On Hemodynamics In Hypertensionmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Endogenous nitric oxide on arterial hemodynamics: a comparison between normotensive and hypertensive rats

American Journal of Physiology-Heart and Circulatory Physiology

1997

Self Cite

Nitric oxide in systemic and pulmonary hypertension

et al. 1997

J Biomed Sci

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Endothelium-derived nitric oxide (NO) is an important gas molecule in the regulation of vascular tone and arterial pressure. It has been considered that endothelial dysfunction with impairment of NO production contributes to a hypertensive state. Alternatively, long-term hypertension may affect the endothelial function, depress NO production, and thereby reduce the dilator action on vasculatures. There were many studies to support that endothelium-dependent vasodilatation was impaired in animals and humans with long-term hypertension. However, results of some reports were not always consistent with this consensus. Recent experiments in our laboratory revealed that an NO synthase inhibitor, N(G)-nitro-L-arginine monomethyl ester (L-NAME) caused elevation of arterial pressure (AP) in spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY). The magnitude of AP increase following NO blockade with L-NAME was much higher in SHR than WKY. In other experiments with the use of arterial impedance analysis, we found that L-NAME slightly or little affected the pulsatile hemodynamics including characteristic impedance, wave reflection and ventricular work. Furthermore, these changes were not different between SHR and WKY. The increase in AP and total peripheral resistance (TPR) following NO blockade in SHR were significantly greater than those in WKY, despite higher resting values of AP and TPR in SHR. In connection with the results of other studies, we propose that heterogeneity with respect to the involvement of NO (impairment, no change or enhancement) in the development of hypertension may exist among animal species, hypertensive models and different organ vessels. Our study in SHR provide evidence to indicate that the effects of basal release of NO on the arterial pressure and peripheral resistance are not impaired, but enhanced in the hypertensive state. The increase in NO production may provide a compensatory mechanism to keep the blood pressure and peripheral resistance at lower levels. The phenomenon of enhanced NO release also occurs in certain type of pulmonary hypertension. We first hypothesized that a decrease in NO formation might be responsible for the pulmonary vasoconstriction during hypoxia. With the measurement of NO release in the pulmonary vein, we found that ventilatory hypoxia produced pulmonary hypertension accompanying an increase in NO production. Addition of NO inhibitor (L-NAME), blood or RBC into the perfusate attenuated or abolished the NO release, while potentiating pulmonary vasoconstriction. During hypoxia, the increased NO formation in the pulmonary circulation similarly exerts a compensatory mechanism to offset the degree of pulmonary vasoconstriction.

Beta-adrenergic mechanisms in arterial hemodynamics: A comparison between normotensive and hypertensive rats

1996

J Biomed Sci

The purpose of this study was to determine whether beta-adrenergically mediated cardiovascular functions such as arterial pressure (AP), heart rate (HR), stroke volume (SV), cardiac output (CO), peripheral resistance (R(p)), arterial impedance (Z(c)), mean arterial compliance (C(m)) and pulse wave reflection (P(b)) were altered in the spontaneously hypertensive rat (SHR) compared to the normotensive Wistar Kyoto rat (WKY). In pentobarbital-anesthetized and artificially ventilated rats, the aortic pressure wave was recorded with a high-fidelity Millar sensor, and aortic flow wave with an electromagnetic flow probe. The pressure and flow waves were subjected to Fourier transform so as to analyze impedance spectra. Acute beta-adrenergic blockade was produced by an intravenous injection of propranolol (nonselective) and atenolol (selective beta(1)-blocker) at doses of 2 and 5 mg/kg, respectively. Steady-state parameters were obtained 15-20 min after intravenous administration. The SHR had higher AP, HR, R(p) and Z(c) than the WKY. SV and CO remained unaltered while C(m) was lower. In response to propranolol, the mean AP was increased by 7 mm Hg in the WKY, but did not change in the SHR. Moreover, significant decreases occurred in HR, CO and C(m) in addition to increases in R(p), Z(c) and P(b). These changes between the SHR and WKY were only slight. Atenolol caused decreases in AP, HR and CO in both SHR and WKY, but did not significantly alter the R(p), Z(c), C(m) and P(b). Again, the atenolol-induced changes in AP, HR and CO did not appear to be significantly different between SHR and WKY. The results indicate that beta-adrenergic effects on the heart, Windkessel and resistance vessels are neither greatly enhanced nor impaired during the development of hypertension. In the hypertensive state, significant beta-adrenergic mechanisms still exert tonic vasodilatory effects on the large and small arterial system. Copyright 1996 S. Karger AG, Basel