Antidipsogenic effects of eel bradykinins in the eelAnguilla japonica

2001 ◽  
Vol 281 (4) ◽  
pp. R1090-R1096 ◽  
Author(s):  
Yoshio Takei ◽  
Takamasa Tsuchida ◽  
Zhihong Li ◽  
J. Michael Conlon

A peptide with bradykinin (BK)-like immunoreactivity was isolated from an incubate of heat-denatured eel plasma with porcine pancreatic kallikrein. The purified peptide had the following amino acid sequence: Arg-Arg-Pro-Pro-Gly-Ser-Trp-Pro-Leu-Arg. This decapeptide, named eel [Arg0]BK, was identical to two previously identified BK homologs from cod and trout. High conservation of the BK sequence among distant teleost species suggests an important function in this vertebrate group. Bolus intra-arterial injections of eel [Arg0]BK, BK, and [Arg0]-des-Arg9-BK (1–10 nmol/kg) caused significant ( P < 0.05) inhibition of drinking in seawater-adapted eels. The potency of the inhibition was ranked in the following order: [Arg0]BK > [Arg0]-des-Arg9-BK = BK. The BK peptides also produced an immediate, transient increase followed by a sustained increase in arterial blood pressure and an initial decrease followed by an increase in heart rate. Strong tachyphylaxis occurred for the cardiovascular effect but not for the antidipsogenic effect. The order of the potency of the cardiovascular actions, [Arg0]BK > BK > [Arg0]-des-Arg9-BK, was different from that of the antidipsogenic action. Slow infusions of eel [Arg0]BK in the dose range 1–1,000 pmol · kg−1 · min−1 produced concentration-dependent inhibition of drinking without changes in arterial pressure, plasma osmolality, and hematocrit. At the infusion rate of >100 pmol · kg−1 · min−1, plasma concentrations of angiotensin II, a potent dipsogenic hormone in eels, increased, suggesting an interaction of the kallikrein-kinin and renin-angiotensin systems. In mammals, BK is dipsogenic and vasodepressor, so that our data demonstrate opposite effects on fluid and cardiovascular regulation of BK in the eel and suggest a new physiological role for the kallikrein-kinin system in teleost fish.

2021 ◽  
Vol 14 (3) ◽  
pp. 240
Author(s):  
Jean-Pierre Girolami ◽  
Nadine Bouby ◽  
Christine Richer-Giudicelli ◽  
Francois Alhenc-Gelas

This review addresses the physiological role of the kallikrein–kinin system in arteries, heart and kidney and the consequences of kallikrein and kinin actions in diseases affecting these organs, especially ischemic and diabetic diseases. Emphasis is put on pharmacological and genetic studies targeting kallikrein; ACE/kininase II; and the two kinin receptors, B1 (B1R) and B2 (B2R), distinguished through the work of Domenico Regoli and his collaborators. Potential therapeutic interest and limitations of the pharmacological manipulation of B1R or B2R activity in cardiovascular and renal diseases are discussed. This discussion addresses either the activation or inhibition of these receptors, based on recent clinical and experimental studies.


1979 ◽  
Vol 237 (1) ◽  
pp. E56
Author(s):  
M J McKinley ◽  
D A Denton ◽  
S Hatzikostas ◽  
R S Weisinger

Intravenous infusion of angiotensin II over the dose range 3-20 microgram/h for 15 min caused a dose-dependent reduction in parotid saliva secretion and increase in arterial blood pressure in conscious sheep. The blood levels of angiotensin II contrived by these infusions were probably within the physiological range for sheep. Infusion of angiotensin II (3 microgram/h) into the carotid artery ipsilateral to the parotid gland under study caused greater reduction in saliva secretion rate than an equivalent infusion of angiotensin II into the contralateral carotid artery. This result suggests a direct effect of angiotensin II at the parotid, possibly by a constrictor action on its vasculature or by altering water and electrolyte transport by the gland. In sodium-deplete sheep, intravenous infusion of the angiotensin antagonist saralasin (1 mg/h for 1 h) caused transient increase of saliva flow for 20-30 min. It is suggested that angiotensin II may have a physiological role in regulating parotid saliva secretion during sodium depletion.


1977 ◽  
Author(s):  
M. J. Gallimore ◽  
A. O. Aasen ◽  
E. Amundsen

Plasma protease activity is known to be increased during endotoxin shock and recent studies have indicated that the plasma kallikrein-kinin system becomes activated by circulating endotoxin. Plasma levels of pre-kallikrein kallikrein and kallikrein inhibitors were therefore determined in samples from dogs infused with E. coli endotoxin, using assays with a chromogenic substrate for plasma kallikrein(Chromozyme -PK, Pentapharm, Basle, Switzerland). “Fast-reacting” and “time-dependent” inhibitors of kallikrein were studied using purified human plasma kallikrein. Considerably reduced levels of plasma pre-kallikreiri and increased levels of kallikrein were detected in the late phase of shock and significant reductions in “fast-reacting” and “time-dependent” inhibition of kallikrein was observed. These results show that during endotoxin shock plasma pre-kallikrein becomes activated to kallikrein and indicate that kallikrein inhibitors play an important mediatory role in the pathophysiology of endotoxin shock.


1976 ◽  
Vol 71 (3) ◽  
pp. 325-331 ◽  
Author(s):  
MANABU YAMAMOTO ◽  
L. SHARE ◽  
R. E. SHADE

SUMMARY In an attempt to determine whether prostaglandin E2 (PGE2) can act centrally to affect the release of vasopressin (ADH), the ventriculo-cisternal system of anaesthetized dogs was perfused with PGE2. When PGE2 was perfused at a rate of 76·4 ng/min (0·19 ml/min), the plasma ADH concentration was unchanged. However, perfusion of PGE2 at a rate of 152·8 ng/min (0·19 ml/min) resulted in a significant increase in the plasma ADH concentration from the control value of 9·0 ± 2·2 (s.e.m.) to 18·8 ± 3·9 μu./ml at 10 min and to 41·0 ± 16·7 μu./ml at 30 min after the start of the perfusion. There were no changes in arterial blood pressure, rectal temperature, plasma osmolality, and the plasma concentrations of sodium and potassium. In additional experiments, i.v. injection of indomethacin (2 or 20 mg/kg) decreased the plasma ADH concentration by approximately 50%. Although this finding is consistent with a role of PGE2 in the control of ADH release, it could also have been due to the observed increases in arterial blood pressure and effective left atrial pressure. Plasma renin activity was unchanged in the indomethacin experiments. It is concluded that PGE2 can act in the central nervous system to stimulate ADH release.


1979 ◽  
Vol 32 (3) ◽  
pp. 353
Author(s):  
AM Beal

Haematocrit values, plasma osmolality and the plasma concentrations of sodium, potassium, chloride and insulin were measured in carotid arterial blood before, during and after intravenous infusion of NaCI (0� 5 moll-i) and KCI (0� 5 moll-i) at 2 ml min~l for 105 min into six conscious splenectomized sheep. Hypertonic NaCI infusion was associated with a fall in haematocrit of 1 �30 � 0�10 % (P < 0�001) and no consistent change in plasma insulin concentration occurred during this infusion. Hypertonic KCI infusion caused the haematocrit to increase by 1�70 � 0�39 % (P < 0�001) and the plasma insulin concentration to increase by 60�0� 16�3 jlU ml-1 (P < 0�01). It was concluded that this increase in insulin concentration was caused by elevation of the plasma potassium concentration and was not due to coincident increases in plasma chloride concentration or osmolality. Shrinkage of the extracellular fluid volume during KCI infusion made no major contribution to the increase in insulin concentration which was probably the result of increased release from the pancreas. [Other keywords: hyperkalaemia, hypernatraemia.j


Perfusion ◽  
1998 ◽  
Vol 13 (5) ◽  
pp. 338-345
Author(s):  
Hans-Joachim Schulze ◽  
Hans Peter Wendel ◽  
Martin Kleinhans ◽  
Siegfried Oehmichen ◽  
Herbert Guggenberger ◽  
...  

Perioperative haemodynamic changes leading to severe circulatory problems during open-heart surgery still represent dreaded complications. The aim of this study was to examine the relationship between the use of applied anaesthetic agents and alterations of the contact phase of the intrinsic blood-clotting system, as changes within the kallikrein-kinin system can lead to a fall in blood pressure. In a randomized study, parameters of the kallikrein-kinin system, coagulation and fibrinolysis were determined for 36 patients with aortocoronary bypass operations. The patients had been given either midazolam/fentanyl or propofol/alfentanil to maintain anaesthesia. Perioperative blood pressure values were registered at seven fixed points. The measured values of the factor XIIa-like activity and the kallikrein-like activity suggested a higher activation of the contact phase, when propofol/alfentanil was given. From the start of the extracorporeal circulation (ECC) to the end of the operation, the kallikrein-like activities in the propofol/alfentanil group were significantly higher than those of the midazolam/fentanyl group. Also, the results of the kallikrein inhibition capacity and the indicators of fibrinolysis (t-PA and D-dimers) indicate a stronger activation of the contact phase - at least at the beginning of recirculation - and as a result of it, a stronger fibrinolysis within the propofol/alfentanil group. In addition, the hypotensive side-effects differed significantly between the two groups. Patients receiving propofol/alfentanil needed the triple amount of anti-hypotonicum to maintain the mean arterial blood pressure above 75 mmHg. With the results of this study, a correlation between the application of propofol/alfentanil, contact phase activation, with activation of the kallikrein-kinin-bradykinin system and the observed hypotension, can be presumed.


1992 ◽  
Vol 263 (2) ◽  
pp. R400-R404 ◽  
Author(s):  
S. Comeau ◽  
V. A. Lance ◽  
J. W. Hicks ◽  
J. M. Conlon

Incubation of plasma form the alligator (Alligator mississipiensis) with glass beads in the presence of a kininase inhibitor resulted in the activation of the kallikrein-kinin system and generation of bradykinin-like immunoreactivity. The kinin peptides were purified to homogeneity and were shown to comprise [Thr6]-bradykinin and des-Arg9[Thr6]bradykinin in the molar ratio of approximately 10:1. Bolus injections of synthetic [Thr6]bradykinin into the jugular vein of the anesthetized alligator resulted in a dose-dependent decrease in mean arterial blood pressure. The minimum dose of kinin producing a significant fall in pressure was 0.07 micrograms/kg body wt and the maximum response (25 +/- 6% fall; mean +/- SD, n = 8) was produced by a dose of 0.56 micrograms/kg body wt. The dose producing a half-maximum response was 0.19 +/- 0.08 micrograms/kg. The data indicate that alligator plasma contains all the components of the kallikrein-kinin system found in mammals and suggest that the system may be of physiological importance in the regulation of cardiovascular function in these reptiles.


1990 ◽  
Vol 259 (4) ◽  
pp. R745-R752 ◽  
Author(s):  
K. A. Dickson ◽  
S. B. Hooper ◽  
I. C. McMillen ◽  
R. Harding

Our aim was to determine fetal and maternal endocrine and fluid-balance responses to prolonged loss of amniotic and allantoic fluids in sheep. In seven sheep, amniotic and allantoic fluids were drained [379.1 +/- 20.1 (SE) ml/day] from 107 to 135.3 +/- 0.6 days of gestation (term: 145 days). The results from these sheep were compared with those from seven control sheep. Maternal water intake, urine production, and urine osmolality were not altered by fluid drainage, nor were fetal and maternal arterial blood gases, pH, or plasma osmolalities. Fluid drainage increased amniotic, but not allantoic, fluid osmolality. Maternal plasma cortisol concentration increased with fluid drainage, but maternal plasma concentrations of prolactin and arginine vasopressin were unchanged. Fluid drainage increased prolactin concentrations in fetal plasma and amniotic fluid, but fetal plasma concentrations of cortisol (hydrocortisone), arginine vasopressin, norepinephrine, and epinephrine were unchanged. Our results show that the fetus is capable of maintaining its plasma osmolality despite prolonged loss of fluid from its amniotic and allantoic sacs and that this is associated with alterations in the production rate and the composition of amniotic fluid.


2003 ◽  
Vol 285 (1) ◽  
pp. R1-R13 ◽  
Author(s):  
Alvin H. Schmaier

Understanding the physiological role of the plasma kallikrein-kinin system (KKS) has been hampered by not knowing how the proteins of this proteolytic system, when assembled in the intravascular compartment, become activated under physiological conditions. Recent studies indicate that the enzyme prolylcarboxypeptidase, an ANG II inactivating enzyme, is a prekallikrein activator. The ability of prolylcarboxypeptidase to act in the KKS and the renin-angiotensin system (RAS) indicates a novel interaction between these two systems. This interaction, along with the roles of angiotensin converting enzyme, cross talk between bradykinin and angiotensin-( 1 – 7 ) action, and the opposite effects of activation of the ANG II receptors 1 and 2 support a hypothesis that the plasma KKS counterbalances the RAS. This review examines the interaction and cross talk between these two protein systems. This analysis suggests that there is a multilayered interaction between these two systems that are important for a wide array of physiological functions.


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