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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
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http://dx.doi.org/10.1007/BF02253709 | DOI Listing |
Int J Mol Sci
August 2025
Department of Laboratory Medicine, Faculty of Medicine, Shimane University, 89-1 Enya Cho, Izumo 693-8501, Japan.
Hypertension and obesity are well-established risk factors for chronic kidney disease (CKD). This study investigates the interaction between these two factors in CKD using animal models. Twelve-week-old normotensive Wistar Kyoto (WKY), spontaneously hypertensive (SHR), and stroke-prone spontaneously hypertensive (SHR-SP) rats were fed either a normal diet (control) or a high-fat diet (HFD) for eight weeks.
View Article and Find Full Text PDFCardiovasc Res
August 2025
Department of Pediatrics, University of Alberta.
Aim: Hypertensive disorders of pregnancy (HDP) are characterized by adverse or inadequate maternal cardiovascular adaptations and are associated with poor perinatal outcomes. Iron deficiency (ID) is a common pregnancy complication that elicits numerous cardiovascular adaptations. Though generally considered deleterious in pregnancy, whether ID mitigates or exacerbates maternal cardiovascular dysfunction in HDP has not been investigated.
View Article and Find Full Text PDFAm J Physiol Heart Circ Physiol
August 2025
Department of Health Sciences, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, São Paulo, Brazil.
Ovarian hormone deprivation may exacerbate hypertension-induced cardiac morphofunctional impairments. However, its effects on left ventricular contractility remain unclear. Herein, we investigated the effects of ovariectomy on hemodynamics, cardiac morphology, and function in vivo and ex vivo in isolated hearts of hypertensive rats (Spontaneously Hypertensive Rats, SHR), and compared these effects to those observed in normotensive controls (Wistar Kyoto, WKY).
View Article and Find Full Text PDFFront Pharmacol
July 2025
Department of Pharmacology and Toxicology, College of Medicine, Kuwait University, Kuwait City, Kuwait.
Background: Angiotensin II (Ang II) signaling via angiotensin II type 1 receptor (AT1R) and transactivation of epidermal growth factor receptor (EGFR) enhances vascular smooth muscle cell (VSMC) proliferation and contributes to vascular remodeling evident in spontaneously hypertensive rats (SHR) aorta. Although high-density lipoprotein (HDL) has been shown to lower blood pressure in SHR, the underlying mechanism(s) remain incompletely understood. We propose that HDL attenuates Ang II-AT1R-EGFR signaling and reverses vascular remodeling in SHR.
View Article and Find Full Text PDFMicrovasc Res
November 2025
School of Public Health, Ningxia Medical University, Yinchuan, Ningxia, China. Electronic address:
This study examined the autophagy and apoptosis of vascular endothelial cells in spontaneously hypertensive rats (SHRs) under intermittent heat stress and determined whether the AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR)/Unc-51 like autophagy activating kinase (ULK1) pathway is involved in autophagy regulation. Wistar-Kyoto (WKY) rats were assigned to control (WKY-CN), intermittent heat stress (WKY-8), and continuous heat stress (WKY-24) groups. SHRs were also assigned to three groups: SHR-CN, SHR-8, and SHR-24.
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