Participation of the nitric oxide pathway in cold-induced hypertension

Several mechanisms are known to participate in cold-induced hypertension, but no information exist on the role of the nitric oxide (NO). In the present study, we assessed the participation of nitric oxide in cold-induced hypertension by means of inhibition of NO synthase. Experiments were performed in rats treated with N omega-nitro-L-arginine (L-NNA) injected i.p. at a dose of 25 mg/kg body weight twice a day for four consecutive days. Control animals received saline injections of the same volume. Two days before the experiment, the femoral artery was cannulated for blood pressure recording. Arterial blood pressure was measured at 25 degrees C for 30 min (control period), followed by a 3.5 hour period at 4 degrees C (cold exposure) and, eventually, a last 3 hour period after removal from cold (back to 25 degrees C). In control animals, at 25 degrees C, mean arterial blood pressure was 112.5+/-3.6 mmHg and heart rate was 380+/-3.5 bpm. L-NNA treatment caused an increase in blood pressure to 155.0+/-3.5 mmHg (P<0.01) and in heart rate to 410+/-6.0 bpm (P<0.05). Exposure to cold caused blood pressure to increase up to 131.5+/-3.6 mmHg (P<0.05) in the control group, whereas no significant change could be measured in treated animals. Recovery from cold exposure led to a decrease in blood pressure in control animals, but not in treated animals. These results indicate that NO plays a role in the development of cold-induced elevation of blood pressure.