Stimulation of the Renal Kallikrein-Kinin System by Vasoactive Substances and Its Relationship to the Excretion of Salt and Water1

Mills, Ivor H.; Obika, L. F. O.; Newport, Pamela A.

doi:10.1159/000401661

Cited by 16 publications

(15 citation statements)

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“…The present results therefore demonstrate that the diuretic response to stimulation of atrial receptors remains unchanged despite the complete blockade of generation of angiotensin II and despite the probable changes in the activity of bradykinin resulting from this blockade [Hulthen and Hokfelt, 1978;Mills, Obika and Newport, 1978].…”

Section: Discussionsupporting

confidence: 51%

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Role of Angiotensin II and Bradykinin in the Diuresis Caused by Stimulation of Atrial Receptors

1980

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The diuretic response to stimulation of left atrial receptors, by distending balloons located either at the pulmonary vein-left atrial junctions or in the body of the left atrium, was studied during blockade of the generation of angiotensin II using Two efferent mechanisms are now known to effect the reflex response of an increase in urine flow to stimulation of atrial receptors; an inhibition of activity in the renal nerves and a blood-borne agent [e.g. . The identity of this blood-borne agent is unknown but it can be detected in dog plasma using an in vitro preparation of Malpighian tubules of Rhlodaiuts prolixu.s [Kappagoda, Knapp, Linden, Pearson and Whitaker, 1979]. Whilst there is evidence that it is not the antidiuretic hormone [e.g. Linden, 1976] it is as yet unknown whether angiotensin II or bradykinin, known to influence urine flow [e.g. Barraclough and Mills, 1965], are involved in the diuretic response which is effected by the proposed agent.The present investigation was undertaken to determine whether or not the diuretic response is mediated by either angiotensin II or bradykinin. MethodsTwo animal preparations were used in the present investigation; anaesthetized dogs for stimulation of atrial receptors, and isolated Malpighian tubules of

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Section: Discussionsupporting

confidence: 51%

“…In addition, Mills, Obika and Newport [1978] showed that intra-arterial infusion of angiotensin 1I in to the kidney effects the release of kallikrein. It could be argued that either angiotensin II or bradykinin is involved in the diuretic response to stimulation of left atrial receptors.…”

Section: Discussionmentioning

confidence: 99%

Role of Angiotensin II and Bradykinin in the Diuresis Caused by Stimulation of Atrial Receptors

1980

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“…Indirect effects include those secondary to interference with blood flow distribution, 28 ADH action on the distal nephron 17 ' N and interaction with angiotensin and kallikrein-kinin systems. 30 Direct effects on tubular functions have been demonstrated by Kauker* 1 who observed inhibition of sodium reabsorption after injection of PGEj within the lumen of rat kidney tubules and by Stokes and Kokko" in isolated perfused collecting ducts.…”

Section: Discussionmentioning

confidence: 96%

Effect of salt on prostaglandin metabolism in hypertension-prone and -resistant Dahl rats.

Goldman¹,

Limas²,

Iwai³

1981

Hypertension

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SUMMARY The effect of high salt intake on rascular and renomedullary prostaglandin (PG) synthesis was compared in Sprague-Dawley and salt-sensitive (S) and -resistant (R) Dahl rats. Animals were given a diet containing either 0.6% or 8% NaCI starting at 5 weeks of age, and were sacrificed 6 weeks later. Systolic blood pressure of S rats increased to 220 ± 7 mm Hg but was unaffected in R and Sprague-Dawley rats. Prostaglandin synthesis was studied in aortic rings and renomedullary mlcrosomes using 14 C-arachidonate as substrate.[*H]PGE, degradation was measured in the renocortical cytosol.In Sprague-Dawley and R rats, aortic PGI t synthesis was not affected by high salt intake, while a significant increase compared to animals on 0.6% NaCI (from 608 ± 84 to 992 ± 108 pmoles/60 min, p < 0.05) was noted in S rats. Enhancement of PGI| synthesis in S rats may be secondary to the hypertension.Salt-loading consistently stimulated renomedullary PGE, synthesis in all three animal groups. S rats, however, had the lowest PG synthesis in renal medullas compared to Sprague-Dawley and R rats when placed on either diet. Thus, even after 6 weeks on high salt, S rats did not reach the levels of PGE, synthesis seen in R or Sprague-Dawley rats on regular diet.The activity of cortical 15-hydroxyprostaglandin dehydrogenase was increased by salt-loading in S and Sprague-Dawley, but not in R rats. R rats had lower dehydrogenase activity than the other two groups when placed on either diet.The observed differences in PG synthesis and catabolism will tend to maintain the net output of renal PGs highest in R and lowest in S rats. These differences correlate with the reported differences in renal papillary flow between these two rat strains and may be relevant to their susceptibility or resistance to hypertension in response to salt. Prostaglandins are involved in the • regulation of physiological and biochemical pathways through both sodium balance and vascular smooth muscle which genetic factors exert their influence on blood tone. It is possible that differences in the pattern of pressure (BP) are unclear. Because of the pivotal role renal and vascular prostaglandin metabolism mediate, of the kidney in regulating BP by maintaining sodium in part, the variable response of BP to salt. The study of the role of prostaglandins in salt-induced hypertension has been facilitated by the development of two From the Department of Pathology, Veterans Administration strains of rats, one sensitive (S) and one resistant (R)%S ^JX^$^ffi?^s£% t0 the effects of salt.-Induction of hypertension in S of Medicine, Minneapolis, Minnesota, and the Broolchaven r a t S by a high salt diet is associated with decreased National Laboratories, Upton, New York renal papillary flow, 10 decreased natriuretic capacity,' Supported in part by grants from the American Heart Assocmand increased systemic vascular resistance 7 compared tion, Minnesota Affiliate, and the Veterans Administration t Q R r a t s T h e p r e s e n t stu( Jy explores the possibility P a S S a -S l S...

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“…Most manoeuvres known so far to stimulate kallikrein excretion, including All infusion (Mills et al, 1978), haemorrhagic hypotension and initiation as well as termination of saralasin infusion, appear to influence the balance between pre-and post-glomerular resistance. This balance in turn ultimately determines glomerular filtration rate (Robertson et al, 1972).…”

Section: Discussionmentioning

confidence: 99%

Urinary kallikrein excretion during inhibition of endogenous angiotensin II in the pig

Binder¹,

Maier²,

Rana³

et al. 1986

British J Pharmacology

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1 This study was performed to assess the possible contribution ofendogenous angiotensin II (All) to the regulation of urinary kallikrein excretion. The All antagonist saralasin or the saline vehicle was infused into the aorta above the renal arteries of pigs under halothane-02/N20 anaesthesia. Systemic and renal functional parameters were followed for 140 min and during stimulation of the reninangiotensin system by haemorrhage. 2 Urinary kallikrein excretion, determined as kininogenase activity, was increased immediately upon both initiation and termination of the 2 h saralasin infusion into pigs not subjected to haemorrhage. Renal cortical blood flow (RCBF) was maintained in both saline and saralasin-treated animals at blood pressures as low as 70 mm Hg, while glomerular filtration rate was dissociated during saralasin infusion. As long as RCBF was maintained, urinary kallikrein excretion rate was elevated during the progressive hypotension in both saline and saralasin-treated animals. 3 These findings confirm a close relationship between the maintenance of RCBF and increased activity of the kallikrein-kinin system whether or not All is antagonized, and indicate that during haemorrhage the kallikrein-kinin system is stimulated by a mechanism not involving All.

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Stimulation of the Renal Kallikrein-Kinin System by Vasoactive Substances and Its Relationship to the Excretion of Salt and Water1

Cited by 16 publications

References 0 publications

Role of Angiotensin II and Bradykinin in the Diuresis Caused by Stimulation of Atrial Receptors

Role of Angiotensin II and Bradykinin in the Diuresis Caused by Stimulation of Atrial Receptors

Effect of salt on prostaglandin metabolism in hypertension-prone and -resistant Dahl rats.

Urinary kallikrein excretion during inhibition of endogenous angiotensin II in the pig

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