Endothelial dysfunction in cold-induced hypertensive rats

• Published in: American journal of hypertension 2002-02, Vol.15 (2), p.176-180
• Main Authors: Zhu, Zhiming, Zhu, Shanjun, Zhu, Jijun, van der Giet, Markus, Tepel, Martin
• Format: Article
• Language: English
• Subjects: Acetylcholine - pharmacology; Animals; Aorta - physiopathology; Arterial hypertension. Arterial hypotension; Biological and medical sciences; Blood and lymphatic vessels; Blood Pressure - drug effects; Cardiology. Vascular system; Cold Temperature; cold-induced hypertension; Endothelial dysfunction; Endothelium, Vascular - physiopathology; eNOS; Enzyme Inhibitors - pharmacology; Experimental diseases; Heart Rate; Hypertension - etiology; Hypertension - physiopathology; In Vitro Techniques; Male; Medical sciences; N G-nitro- l-arginine-methyl ester; NG-nitro-L-arginine-methyl ester; NG-Nitroarginine Methyl Ester - pharmacology; nitric oxide; Nitric Oxide Synthase - metabolism; Nitric Oxide Synthase Type III; Rats; Rats, Wistar; Vasodilator Agents - pharmacology
• ISSN: 0895-7061; 1879-1905; 1941-7225
• DOI: 10.1016/S0895-7061(01)02268-3

Endothelial dysfunction can be observed in preatherosclerotic conditions. However, its pathogenetic role in hypertension is still controversial. Endothelial-dependent changes of blood pressure (BP) and expression of endothelial nitric oxide synthase (eNOS) were evaluated in cold-induced hypertensive rats. Wistar rats were exposed to cold stress for 8 weeks. Exposure to cold stress significantly increased the systolic BP in rats. The infusion of acetylcholine significantly lowered mean arterial BP in control rats by 48 ± 2% and by 32 ± 1% in cold-induced hypertensive rats. The acetylcholine-induced reduction of mean arterial BP was significantly attenuated in cold-induced hypertensive rats (control rats, 45 ± 2 mm Hg; cold-induced hypertensive rats, 34 ± 3 mm Hg; P < .05). Administration of NG-nitro-L-arginine-methyl ester for 1 week significantly increased BP in control rats, whereas no effect could be observed in cold-induced hypertensive rats. In cold-induced hypertensive rats eNOS in aortic vessels was significantly reduced compared to control rats. In this nongenetic, nonsurgical animal model of cold-induced hypertensive rats an endothelial dysfunction can be observed due to reduced eNOS.