The role of the sympathetic nervous system in arterial hypertension cannot be properly evaluated until we know about its activity in the vessels themselves. In this study we investigated the effect of transmural stimulation on the tail artery - labelled in vitro with 3H-norepinephrine - of 7-9 week old spontaneously hypertensive rats (SHR) and Wistar Kyoto controls (WKR). Electrical stimulation using two frequencies (2 and 10 Hz) resulted in significantly more 3H overflow in vessels from SHR than from WKR. With 10 Hz stimulation the fractional release was also greater. Column chromatographic analysis of 3H overflow revealed that transmural stimulation in arteries of SHR enhanced mainly the release of norepinephrine and not of its metabolites. Significantly, an increased release of 3H-norepinephrine on stimulation was observed in SHR before the full development of hypertension suggesting that it might be a cause rather than a consequence of high blood pressure.

1 The effects of diltiazem in rat tail arteries and guinea-pig vasa deferentia have been investigated. 2 Superfusion of the rat tail artery with diltiazem (10-6 10-M) resulted in a dose-related increase in 3H-overflow (P < 0.001) both in Wistar Kyoto (WKY) and in spontaneously hypertensive (SHR) rats. Release of 3H by transmural stimulation (I Hz, 2 ms, 10 V) was also much greater in vessels perfused with diltiazem; this effect was dose-dependent. 3 Diltiazem did not significantly alter the proportion of noradrenaline and its metabolites in 3H-overflow, as analysed by column chromatography. 4 In the vasa deferentia of guinea-pigs, diltiazem (10--10-M) increased spontaneous 3H-release. 5 The results indicate that diltiazem acts on sympathetic nerves and causes the release of noradrenaline.

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