Noradrenaline as a possible mediator of the actions of angiotensin on fluid transport by rat rejunum <i>in vivo</i>

Levens, Nigel; Munday, K. A.; Parsons, B. J.; Poat, Judith A.; Stewart, C. P.

doi:10.1113/jphysiol.1979.sp012624

Cited by 29 publications

(17 citation statements)

References 15 publications

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“…While substantial evidence is available indicating noradrenergic mediation ofAII-induced ion transport in vivo (Levens et al, 1979;1981) none of the a-or Padrenoceptor antagonists tested in the present study affected All responses in either the jejunum or colon. Yohimbine and phentolamine did, however, block NA-induced reductions in SCC in preparations of jejunum in agreement with an x2-adrenoceptor mechanism of action described by Chang et al (1982).…”

Section: Discussioncontrasting

confidence: 64%

The effect of angiotensin II upon electrogenic ion transport in rat intestinal epithelia

Cox

Cuthbert

Munday

1987

British J Pharmacology

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Epithelial sheets from rat jejunum and descending colon have been shown to respond to angiotensin II (AII) when studied under short‐circuit conditions and bathed on both sides with Krebs‐Henseleit solution. The octapeptide AII elicited increases in short‐circuit current (SCC) in preparations of jejunum and decreases in SCC in the descending colon; both responses occurred when the peptide was applied to the basolateral surface, but not when applied to the apical solution. Responses in both tissues were highly specific, being inhibited by a range of AII antagonists with the following order of potency: [Sar1. Thr8]‐AIi>[Sar1. Leu8]‐AIi>[Sar1. Ile8]‐AIi>[Sar1. Ala8]‐AIi>[Des, Asp1. Ile8]‐AII in rat jejunum. AII responses were not affected by α‐or β‐adrenoceptor antagonists, atropine or tetrodotoxin. AII responses were totally inhibited by the chloride channel blocker, diphenylamine‐2‐carboxylate (DPC) while cotransport inhibitors e.g. piretanide and frusemide significantly reduced the size of AII responses in colon and jejunum. These patterns of activity suggest that in the jejunum the responses result from electrogenic chloride secretion. Although AII responses in colon were sensitive to DPC the transporting ions have not yet been identified. Both piroxicam and indomethacin inhibited the increase in SCC elicited by AII in the jejunum, and the reduction in SCC caused by AII in the colon. Taken together these results indicate that eicosanoids are involved in AII responses in both tissues. This is the first study to demonstrate a direct, electrogenic effect for AII on transporting epithelia from the gastrointestinal tract. The responses are most probably initiated by AII interacting with previously identified specific AII receptors within the epithelial membranes.

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Section: Discussioncontrasting

confidence: 64%

The effect of angiotensin II upon electrogenic ion transport in rat intestinal epithelia

Cox

Cuthbert

Munday

1987

British J Pharmacology

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“…It is well-known that after denervation effector organs become supersensitive to the effects of endogenous neurotransmitter (24). Because exogenous norepinephrine exhibits a dose-dependent dual action on jejunal water transport (9), it is possible in our sympathectomy experiments that denervation supersensitivity could have altered responses ofthe jejunum to endogenously released norepinephrine. However, angiotensin II failed to stimulate jejunal transport at any dose in sympathectomized rats or animals acutely treated with guanethidine.…”

Section: Discussionmentioning

confidence: 86%

“…7). Phentolamine (36 ,g/kg per min) abolishes the stimulation of jejunal water absorption and the associated increase in systemic blood pressure produced by infusion of 7 nmol/ kg per min norepinephrine (9). Similarly, in the present study, pretreatment of the animals with prazosin (200 ,ug) attenuated the increase in blood pressure in response to 7 nmol/kg per min norepinephrine (88±9.0 -151+4.0 to 71+4.9-91+4.0 mm Hg).…”

Section: Resultsmentioning

confidence: 99%

Interactions between angiotensin peptides and the sympathetic nervous system mediating intestinal sodium and water absorption in the rat.

Levens¹,

Peach²,

Carey³

1981

J. Clin. Invest.

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“…Although this effect was blocked by ouabain at 2.5 ng/ml, this level ofouabain Biochemistry: Brock et aL is probably too low to inhibit the Na+/K' pump in rat.tissues (35). Angiotensin peptides are potent stimulators of intestinal Na and water absorption; however, this effect ofAII was shown to be due to the release of norepinephrine from nerve endings in the jejunum (36)..The Na+/K+-ATPase activity ofmicrosomal membranes prepared from certain tissues, but not others, was increased when assayed in the presence of AII (37)(38)(39). Alr though membranes from vascular smooth muscle were not included in previous studies (37-39), we have found that AII had no significant effect on the Na+/K+-ATPase activity in membranes isolated from the smooth muscle cultures (unpublished data).…”

Section: Discussionmentioning

confidence: 99%

Angiotensin increases Na+ entry and Na+/K+ pump activity in cultures of smooth muscle from rat aorta.

Brock¹,

Lewis²,

Smith³

1982

Proc. Natl. Acad. Sci. U.S.A.

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Angiotensin markedly altered the Na' permeability of smooth muscle cells cultured from explants of rat aorta. The rate ofnet Na' uptake was followed in the presence ofouabain in order to block Na' efflux via the Na+/K' pump. Angiotensin H (All) or angiotensin m (AHI) increased net Na' uptake by about 3-fold. Maximal stimulation of Na' uptake was produced by about 10 nM AUl. Bradykinin and the angiotensin antagonist [Sari, Ileu5, Ala8JAII had no significant effect on net Na+ uptake. Angiotensin also enhanced the activity of the Na+/K+ pump, which was assayed by following the rate of ouabain-sensitive wRb+ uptake by the cells. AII and AI nearly doubled ouabain-sensitive 86Rb+ uptake, but bradykinin, norepinephrine, and [SariIleu5,Ala8]AII had no effect. In the presence of ouabain, 86Rb+ uptake was not significantly affected by AUl or AM, indicating that angiotensin did not alter passive permeability to Rb+. Loading the cells with Na+, either by incubation in K+-free medium or exposure to the Na+-selective ionophore monensin, markedly increased ouabainsensitive 86Rb+ uptake. This result indicates that the activity ofthe Na+/K+ pump is limited by the low level of Na+ that is normally in the cells. All had no effect on the activity of the Na+/K+ pump in Na+-loaded cells. These results suggest that All or AIM stimulates the Na+/K+ pump in cultured aortic muscle cells by increasing its Na+ supply.The octapeptide hormone angiotensin II (All) is a highly potent vasoconstrictor (1-3). Specific receptors on the surface of smooth muscle cells (4) mediate the contractile response to All, which occurs when the level of free Ca2" in the cytoplasm increases (5, 6). It is unclear what transmembrane events are elicited when All binds to its receptor on the cell surface.All is known to depolarize the smooth muscle membrane in various tissues (7)(8)(9). Recently, Hamon and Worcel (9) reported evidence suggesting that All depolarizes uterine smooth muscle by increasing the conductance of the membrane to Na+. Alterations in Na+ permeability also appear to be involved in vasoconstriction by angiotensin. Increasing the Na+ concentration in the medium bathing segments of rat aorta potentiates the contractile response to All (10), and perfusing rat tail arteries with low Na+ decreases the constriction elicted by All (11). However, the reported influences of angiotensin on the Na+ movements in isolated vascular tissue are ambiguous. Although Friedman and Allardyce (12) reported that angiotensin decreased the Na' activity in the medium bathing an artery, Guignard and Friedman (13) found that pressor doses ofAll had no such effect.All was recently shown to stimulate phosphorylation of the 20,000-dalton light chain of myosin in primary cultures of vascular smooth muscle (14). Therefore, it is feasible to study vasoactive mechanisms in cultured cells. In an attempt to elucidate further the effects of angiotensin on cation transport, we have examined the influence of vasoactive agents on Na' and K+ movements in cultures of rat aor...

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Noradrenaline as a possible mediator of the actions of angiotensin on fluid transport by rat rejunum in vivo

Cited by 29 publications

References 15 publications

The effect of angiotensin II upon electrogenic ion transport in rat intestinal epithelia

The effect of angiotensin II upon electrogenic ion transport in rat intestinal epithelia

Interactions between angiotensin peptides and the sympathetic nervous system mediating intestinal sodium and water absorption in the rat.

Angiotensin increases Na+ entry and Na+/K+ pump activity in cultures of smooth muscle from rat aorta.

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