Evidence for (Na+Cl) cotransport in rat arterial smooth muscle and its role in contractility

Evidence for (Na+Cl) cotransport in rat arterial smooth muscle and its role in contractility

$26 Abstracts / Comparative Biochemistry and Physiology, Part A 126 (2000) SI SI63 COMPUTATION OF FLOW AROUND A SWMMING ANIMAL Cheng J-Y. and Chahin...

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$26

Abstracts / Comparative Biochemistry and Physiology, Part A 126 (2000) SI SI63

COMPUTATION OF FLOW AROUND A SWMMING ANIMAL Cheng J-Y. and Chahine G.L. D y n a f l o w , Inc., 7 2 1 0 P i n d e l l S c h o o l R o a d , F u l t o n , M a r y l a n d 2 0 7 5 9 , U S A The external morphology and propulsive movement pattern adopted by swimming animals are critical in realizing the highefficiency and high-performance aquatic locomotion, however, their modelling and simulation are challenging in solving the involved hydrodynamic problems. Analytical and numerical slender body and thing wing theories have been used to study fish swimming of constant speeds and of simplified shapes. Recently, there are also efforts to numerically solve Navier-Stoke equation for aquatic locomotion, however the success is still limited by the current capability of the NSequation based CFD. The flow around the body, and the structure and dynamic behaviour of vortex wake generated by swimming animals are responsible for the underlying fluid dynamic mechanisms for reducing wake energy loss, minimizing drag and noise, maintaining sufficient thrust for cruising, and generating rotating moment for rapid manoeuvring. A time-domain 3-D boundary element method (BEM) based on potential flow theory has been developed, which is able to model more realistic geometries and the time-dependent body deformations. The scheme allows the large amplitude movement of tail, fins, and body, and the flow interaction between fins and body. It can efficiently compute much of the flow field around the animal and capture the evolution of the large vortex structures in the flow field. The BEM formulation is based on Green Identity and employs both source and dipole singularities on the discretized surface boundaries. Thus, the computational dimension of the problem is reduced by one, while the 3-D physics is retained. This results in significant saving in computational memory and CPU time requirements. A BEM code, 3DYNAFS, has been developed at DYNAFLOW for modelling the bubble dynamics, ocean surface wave dynamics, and the interaction with surrounding structures. This code is being extended to model the unsteady movement of the body and its wake evolution. The validation and verification of the code have been conducted to ensure the accuracy of the method for the computation of the swimming flow. Result is obtained for a caudal fin performing large-amplitude heave-pitch motion, representing carangiform/lunate tail swimming, and an undulating body with tail, resembling the anguilliform/carangiform swimmer. 3D pressure distribution over the body surface, vorticity in the wake, and the velocity field around the body are computed and analysed.

EVIDENCE FOR (NA+CL) C O T R A N S P O R T IN RAT ARTERIAL SMOOTH MUSCLE AND ITS ROLE IN CONTRACTILITY Chipperfield A.R. and Harper A.A. Department of Anatomy and Physiology, University of Dundee, Dundee DD 1 4HN, UK Rat femoral arteries were mounted in a Mulvany-Halpern wire myograph and the smooth muscle impaled with a conventional K-acetate filled microelectrode. The membrane potential was -66.0 +_ 0.0 (s.d, n = 4) mV in 5 mM [K]o. When the artery was precontracted by increasing [K]o to 40 mM, Em fell to -24.5 + 0.8 (n = 3) mV and the arteries generated a force of 10.4 - 21.8 mN. Metolazone, an inhibitor of (Na+CI) cotransport, was then applied as a nominally saturated solution of - 30 >M. This E m t o 3 5 . 0 --- 1.4 (n = 3) and the force fell by 5.6 _+ 1.0 (n = 4) raN. Similarly, in 30 mM [K]o, Em hyperpolarised from -31.8 -4- 4.9 (n = 4) mV to ~46.5 + 0.7 (n = 3) with metolazone and the force fell by 14.0 + 9.8 mN. Metolazone also relaxed the artery when it was precontracted with phenylephrine and when the endothelium had been destroyed.

hyperpolarised

In the quiescent smooth muscle, there is no evidence of (Na+CI) cotransport (Davis, 1996) but it appears to be activated by depolarisation so that when it is inhibited [C1]i falls, Em hyperpolarises and the artery relaxes in the same way that inhibition of (Na+K+CI) cotransport causes relaxation (Kreye et a1.1981) and any other manoeuvre that attenuates the influence of [C1]i on Em (Bannister et al. 1999). Bannister et al. (1999) J.Physiol. 520P, 99P. Davis, J.P.L (1996) J.Physiol. 491, 61-68. Kreye,V.A.W. et al. (1981) Eur.J.Pharmacol. 73, 91-95.