1. The respective role of alpha-adrenergic and beta-adrenergic receptors in mediating the effect of catecholamines on renin secretion was examined in the isolated perfused rat kidney.

2. Noradrenaline, which has combined alpha- and beta-adrenergic activity, stimulated renin secretion only in the presence of the alpha-receptor blocking agent phenoxybenzamine. This stimulatory effect was largely prevented by the addition of the beta-blocking agent, propranolol. The vasoconstrictor action of noradrenaline, and thus the rise in mean renal perfusion pressure, was abolished by phenoxybenzamine. Our previous finding that noradrenaline alone stimulated renin release was inconclusive (Vandongen, Peart & Boyd, 1973).

3. Noradrenaline stimulated renin secretion when calcium was excluded from the perfusion fluid, to which disodium EDTA (25 mmol/l) was added. The vasoconstrictor action of noradrenaline was considerably attenuated under these conditions.

4. Methoxamine, which has only alpha-adrenergic activity, did not increase renin secretion when infused alone or with phenoxybenzamine. The increase in renin secretion after beta-adrenergic stimulation with isoproterenol was significantly suppressed by methoxamine, although this was associated with an increase in mean renal perfusion pressure.

5. These findings indicate the importance of intrarenal beta-adrenergic receptors in the stimulation of renin secretion and suggest that an opposite inhibitory effect on renin secretion follows alpha-adrenergic activity.

6. Although the results do not exclude a direct effect of vascular tone and renal perfusion pressure, it is suggested that the stimulation and inhibition of renin secretion is related to smooth muscle activity by the involvement of a calcium-dependent process similar to that involved in contraction and relaxation. This would accord with the common derivation of the renin-producing and vascular smooth muscle cells

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