A high salt diet in some species results in elevated arterial blood pressure and alterations in vascular smooth muscle responses to agonists. Weanling male Sprague‐Dawley rats were given either a high salt diet containing 8 % or a low salt diet of 0.4 % sodium chloride for a period of 4 weeks. At the end of the feeding period, tail systolic pressure was higher in the high salt than in low salt rats. The rats were then killed and the intestines removed. Vascular smooth muscle (VSM) responses were estimated from the changes in lumenal diameter of pressurised second order mesenteric resistance arteries. High salt diet resulted in enhanced VSM responses to noradrenaline. The vessels dilated in response both to acetylcholine and to sodium nitroprusside and the responses were similar in vessels from both high and low salt rats. However, vessels from high salt rats were resistant to the blocking of endothelium derived nitric oxide (EDNO) with L‐NAME and the responses were instead abolished by blocking endothelium derived hyperpolarising factor (EDHF) with apamin and charybdotoxin. These results show that in Sprague‐Dawley rats, a high salt diet enhances the vasoconstriction in response to noradrenaline. The vasodilatory responses to acetylcholine were not significantly changed. However, they appeared to be mediated mainly by EDHF rather than by EDNO as in the low salt animals.

We stimulated the aortic chemoreceptors in dogs that were anesthetized with chloralose and artificially ventilated by perfusing the isolated aortic arch with venous blood. Inotropic responses were determined by measuring the maximum rate of change of left ventricular pressure (dP/dt max) with aortic pressure and heart rate held constant. Stimulation of the aortic chemoreceptors resulted in an average increase in heart rate of 14 +/- 2.0 beats/min (mean +/- SE) from 166 +/- 7.7 beats/min and an increase in dP/dt max of 501 +/- 85 mm Hg/sec from 3508 +/- 154 mm Hg/sec. These changes were statistically significant (P less than 0.001). The afferent pathway of the reflex was shown to be in the vagus nerves and the efferent pathway in the cardiac sympathetic nerves. In some of the dogs, the carotid chemoreceptors were also stimulated. This resulted in decreases in heart rate and dP/dt max of 48 +/- 24 beats/min and 795 +/- 142 mm Hg/sec. Thus we have shown that stimulation of aortic chemoreceptors evokes chronotropic and inotropic responses opposite to those evoked from stimulation of carotid chemoreceptors.

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The effect of sex hormones on vascular reactivity is considered one of the underlying factors contributing to gender differences in cardiovascular functions and diseases. Experiments were designed to investigate the role of androgens in salt-induced hypertension by assessing the relaxation response of isolated aortic rings to acetylcholine and sodium nitroprusside in the presence or absence of l-nitroarginine methyl ester in Sprague-Dawley rats. The rats were either orchidectomized or sham-operated, with or without testosterone replacement, and were placed on a normal or high-salt diet for 6 weeks. The results indicate a significant increase (p < 0.001) in the mean arterial blood pressure of rats on the high-salt diet, when compared with control or orchidectomized rats. Orchidectomy elicited a reduction in mean arterial blood pressure (p < 0.01), while testosterone replacement normalized mean arterial blood pressure to values seen in intact rats on the high-salt diet. The high-salt diet reduced the relaxation response to acetylcholine both in the presence and absence of inhibition of endothelial nitric oxide synthase with l-nitroarginine methyl ester. Bilateral orchidectomy attenuated the impaired endothelial function induced by the high-salt diet in rats, but this was reversed by concomitant administration of testosterone, suggesting a role for androgens in enhancing long-term vascular smooth muscle tone and hence maintenance of high blood pressure in salt-induced hypertension.

1. The present study examined the effects of concurrent manipulation of dietary calcium and salt on contractile responses of vascular smooth muscle (VSM) and endothelial function of aortic rings from Sprague-Dawley rats. 2. Salt loading enhanced the contractile response of the aortic rings to noradrenaline (NA), an effect that was blunted by a high calcium intake. 3. Removal of the endothelium and incubation of aortic rings in physiological salt solution containing methylene blue increased the sensitivity of the rings to NA. 4. The increase in the sensitivity of aortic rings induced by endothelium removal was more pronounced in aortic rings from salt-loaded rats. 5. Acetylcholine caused similar degrees of relaxation in all experimental groups, but the relaxation to histamine was smaller (P < 0.05) in salt-loaded rats than in other groups of rats; however, after removal of the endothelium, the contractile response to histamine was higher in salt-loaded rats. 6. The results indicate that the hypersensitivity of isolated aortic rings to agonists, as observed in salt-loaded rats, is due to altered responses of the VSM and not as a result of changes in the endothelium. In addition, salt loading tends to increase the synthesis of endothelium-dependent relaxing factor. The ability of salt loading to enhance the contractile responses of VSM to agonists can be prevented by supplementing the diet with high calcium.