698 Gliicose Adrian et al.’ found no increase in plasma-p.p. during the first 60 min in response to infusion with glucose (20 g glucose during 30 min). However, Floyd et al. found a significant increase in response to parenteral glucose (30 g glucose, 60 min) and a considerable increase in P.P. concentrations during the fourth and fifth hour of an oral glucose test.
of P.P. release in response to food (though this did not quite reach statistical significance in our data) and that the first phase is more under vagal influence. In conclusion, we are glad of this confirmation of our data and agree that the entero-p.p. axis is probably mediated by the synergistic action between intestinal hormones and the vagus, The urgent need now is to find out what P.P. does.
Secretin The P.P. response to intravenous Boots secretin, demonstrated by Adrian et al.,’ cannot be interpreted as mediation by secretin, because Boots secretin contains several hormones. This result shows only that some gut factor(s) may release P.P., since highly purified secretin does not by itself release p.p.66
Department of Medicine, Royal Postgraduate Medical School,
Ccerulein Adrian et al.’ found no increase in plasma-p.p. during infusion with aminoacids (25 g in 250 ml during 30 min). Floyd et all found a significant increase in response to infusion of a mixture of ten essential aminoacids (2-9 mmol/kg during 30 min) but not in response to arginine. These differences in results cannot be attributed to antibody specificity since all P.P. assays make use of the same antiserum (kindly supplied by Dr R. E. Chance, Eli-Lilly, Indianapolis). The P.P. response during a meal is biphasic.4 This biphasic response has been reproduced by Adrian et al. (ref. 1, fig. 1, and ref. 8, fig. 4), though seemingly unnoticed by them. We believe that the initial, very rapid P.P. response duringa meal is almost entirely dependent on vagal activity, and that the secondary, prolonged P.P. response is due to synergistic action of intestinal hormones, vagal activity, and, possibly, absorbed aminoacids. Institute of Medical
Biochemistry, University of Aarhus, 8000-DK Aarhus C, Denmark
S. R. BLOOM T. E. ADRIAN
London W12
ADRENERGIC RECEPTORS AND RENIN RELEASE
StR,—The dominant role of the sympathetic nervous system in the control of renin release has been demonstrated by Davies and Slater.’Buhler et al. have suggested that the reninsuppressing effects of &bgr;-adrenergic-receptor-blocking drugs constitute the primary mechanism of their antihypertensive effect,2 and it has been suggested that the receptors mediating renin release are of the p, type. Problems with methodology, which lead to inactive renin being assayed along with active
THUE W. SCHWARTZ JENS J. REHFELD
This letter has been shown to Dr Bloom and his colleagues, whose
reply follows.-ED. L.
SiR,—Dr Schwartz and Professor Rehfeld state that our results are controversial. We feel, however, that, considering the newness of this area of research, considerable unanimity has been achieved. The release of P.P. by gut hormones (point 5) accords with our own finding. Dr Schwartz and Professor Rehfeld mention (point 4), as we did, that Boots secretin is impure. We ourselves have found that pure secretin is a very poor releaser of P.P. They cite (point 3) unpublished results of Floyd et al. who apparently also found no change in P.P. in the first hour after administration of intravenous glucose. The response to aminoacids (point 2) is clearly variable and depends on the exact stimulus used. Floyd et al. seem to have found some rise with a slightly larger total quantity than we used, and this would certainly give supraphysiological plasma concentrations of the ten aminoacids used. We agree (point 1) that the vagus is one of the important mechanisms for P.P. release, as we demonstrated with the large release of P.P. in non-vagotomised subjects during insulin hypoglycsemia. The analysis of the postprandial release of P.P. after vagotomy is more difficult, however. Dr Schwartz and Professor Rehfeld claim that it is better to use the individual patient as his own preoperative control. A major problem here, however, is that gastric emptying is very abnormal for some months after vagotomy and pyloroplasty. It might be this, rather than absence of vagal innervation as such, that caused their delayed release of P.P. They state, however, that there is a rather small numerical difference between preoperative and postoperative data on the secondary P.P. response after vagotomy, obscured in their data by the presence of two duodenal-ulcer patients with high P.P. levels. It is certainly feasible that there is a biphasic response 8.
Adrian, T. E., Bloom, S. R., Bryant, M. G., Polak, J. M., Heitz, P. H., barnes, A. J. Gut, 1976, 17, 940.
-
-
0 min.
30
Plasma-angiotensin-II (meam±S.E.M.) before
and after acebu-
tolol. cast doubt on this classification. We have studied the effects of the p, selective antagonist acebutolol (25 mg intravenously) on plasma-angiotensin-n levels in nine patients with essential hypertension. Angiotensin it was measured by the radioimmunoassay method of Dusterdieck and McElwee.4 Plasma-angiotensin-u levels depend directly on invivo renin activity, and methodological problems are therefore avoided. Blood-samples were taken before acebutolol infusion and 30 and 120 min afterwards. The results (see (time figure) show that acebutolol induced a sharp fall in plasmaangiotensin-n at both 30 and 120 min (P
of P.P. release in response to food (though this did not quite reach statistical significance in our data) and that the first phase is more under vagal influence. In conclusion, we are glad of this confirmation of our data and agree that the entero-p.p. axis is probably mediated by the synergistic action between intestinal hormones and the vagus, The urgent need now is to find out what P.P. does.
Secretin The P.P. response to intravenous Boots secretin, demonstrated by Adrian et al.,’ cannot be interpreted as mediation by secretin, because Boots secretin contains several hormones. This result shows only that some gut factor(s) may release P.P., since highly purified secretin does not by itself release p.p.66
Department of Medicine, Royal Postgraduate Medical School,
Ccerulein Adrian et al.’ found no increase in plasma-p.p. during infusion with aminoacids (25 g in 250 ml during 30 min). Floyd et all found a significant increase in response to infusion of a mixture of ten essential aminoacids (2-9 mmol/kg during 30 min) but not in response to arginine. These differences in results cannot be attributed to antibody specificity since all P.P. assays make use of the same antiserum (kindly supplied by Dr R. E. Chance, Eli-Lilly, Indianapolis). The P.P. response during a meal is biphasic.4 This biphasic response has been reproduced by Adrian et al. (ref. 1, fig. 1, and ref. 8, fig. 4), though seemingly unnoticed by them. We believe that the initial, very rapid P.P. response duringa meal is almost entirely dependent on vagal activity, and that the secondary, prolonged P.P. response is due to synergistic action of intestinal hormones, vagal activity, and, possibly, absorbed aminoacids. Institute of Medical
Biochemistry, University of Aarhus, 8000-DK Aarhus C, Denmark
S. R. BLOOM T. E. ADRIAN
London W12
ADRENERGIC RECEPTORS AND RENIN RELEASE
StR,—The dominant role of the sympathetic nervous system in the control of renin release has been demonstrated by Davies and Slater.’Buhler et al. have suggested that the reninsuppressing effects of &bgr;-adrenergic-receptor-blocking drugs constitute the primary mechanism of their antihypertensive effect,2 and it has been suggested that the receptors mediating renin release are of the p, type. Problems with methodology, which lead to inactive renin being assayed along with active
THUE W. SCHWARTZ JENS J. REHFELD
This letter has been shown to Dr Bloom and his colleagues, whose
reply follows.-ED. L.
SiR,—Dr Schwartz and Professor Rehfeld state that our results are controversial. We feel, however, that, considering the newness of this area of research, considerable unanimity has been achieved. The release of P.P. by gut hormones (point 5) accords with our own finding. Dr Schwartz and Professor Rehfeld mention (point 4), as we did, that Boots secretin is impure. We ourselves have found that pure secretin is a very poor releaser of P.P. They cite (point 3) unpublished results of Floyd et al. who apparently also found no change in P.P. in the first hour after administration of intravenous glucose. The response to aminoacids (point 2) is clearly variable and depends on the exact stimulus used. Floyd et al. seem to have found some rise with a slightly larger total quantity than we used, and this would certainly give supraphysiological plasma concentrations of the ten aminoacids used. We agree (point 1) that the vagus is one of the important mechanisms for P.P. release, as we demonstrated with the large release of P.P. in non-vagotomised subjects during insulin hypoglycsemia. The analysis of the postprandial release of P.P. after vagotomy is more difficult, however. Dr Schwartz and Professor Rehfeld claim that it is better to use the individual patient as his own preoperative control. A major problem here, however, is that gastric emptying is very abnormal for some months after vagotomy and pyloroplasty. It might be this, rather than absence of vagal innervation as such, that caused their delayed release of P.P. They state, however, that there is a rather small numerical difference between preoperative and postoperative data on the secondary P.P. response after vagotomy, obscured in their data by the presence of two duodenal-ulcer patients with high P.P. levels. It is certainly feasible that there is a biphasic response 8.
Adrian, T. E., Bloom, S. R., Bryant, M. G., Polak, J. M., Heitz, P. H., barnes, A. J. Gut, 1976, 17, 940.
-
-
0 min.
30
Plasma-angiotensin-II (meam±S.E.M.) before
and after acebu-
tolol. cast doubt on this classification. We have studied the effects of the p, selective antagonist acebutolol (25 mg intravenously) on plasma-angiotensin-n levels in nine patients with essential hypertension. Angiotensin it was measured by the radioimmunoassay method of Dusterdieck and McElwee.4 Plasma-angiotensin-u levels depend directly on invivo renin activity, and methodological problems are therefore avoided. Blood-samples were taken before acebutolol infusion and 30 and 120 min afterwards. The results (see (time figure) show that acebutolol induced a sharp fall in plasmaangiotensin-n at both 30 and 120 min (P
