Artery relaxation

Simonsen s group has performed some elegant work over the years on NO release characteristics from rat superior mesenteric artery. Initially, Simonsen s group simultaneously monitored artery relaxation and NO concentration in the artery using a NO microsensor in response to various drugs [120], NO concentration was monitored via an ISONOP30 electrode, purchased from WPI and inserted into the artery lumen using... 

FIGURE 1.7 Simultaneous measurements of force (upper traces) and NO concentration (lower traces) in an endothelium intact (+E) segment of rat superior mesenteric artery contracted with 0.5 J,M noradrenaline (NA) and relaxed with either 10pM acetylcholine (ACh) (a), or 10 pM SNAP (b). Panel C shows a similar measurement in the rat superior mesenteric artery after mechanical endothelial cell removal. As can be seen in C, ACh addition does not cause NO production from the artery but shows an NO increase upon SNAP addition causing artery relaxation. W = washout. (Reprinted with permission from Blackwell Publishing [120].)... 

Kugiyama K, Kerns SA, Morrisett JD, Roberts R, Henry PD (1990) Impairment of endothelium-dependent arterial relaxation by lysolecithin in modified low-density lipoproteins. Nature 344 160-162... 

Nelson I would like to return to what David Eisner mentioned about the plasma membrane determining the steady-state free Ca2+, and what Rick Paul said about sparks and long-conductance Ca2+-dependent K+ (BK) channels. We have looked at cerebral arteries from PLB knockout mice. The spark frequency and the associated transient BK current frequency are elevated by about a factor of three. SR load goes up, the membrane potential hyperpolarizes and the artery relaxes. It would be useful to measure membrane potential under all the conditions as well as determine the voltage dependence of tone, to make sure that your manipulations are not simply changing the membrane potential. 

Nelson We can induce waves, and add a Ca2+ channel blocker. The average Ca2+ goes down, the arteries relax and the waves continue on. 

Nelson Gil Wier, in your paper with Mordy Blaustein, you applied Ca2+ channel blockers, the arteries relaxed and the waves continued, didn t they ... 

A much milder and legal stimulant is caffeine, depicted in Figure 14.27. A number of mechanisms have been proposed for caffeines stimulatory effects. Perhaps the most straightforward mechanism is caffeine s facilitating of the release of norepinephrine into synaptic clefts. Caffeine also exerts many other effects on the body, such as dilation of arteries, relaxation of bronchial and gastrointestinal muscles, diuretic action on the kidneys, and stimulation of stomach-acid secretion. 

Gonadorelin inhibits nitric oxide-mediated arterial relaxation, which disappears within 3 months after stopping treatment. This effect was abolished with add-back hormone replacement in a prospective, randomized study of 50 women treated for 6 months (6). 

Inhibitory effects of high concentrations of LDL (2000 pg/ml) on endothelium-dependent arterial relaxation have been reported by Andrews et al. [119]. These authors suggested that the effects are mediated by an apolipoprotein receptor mechanism involving native LDL. 

Vedernikov, Y.P., Graser, T., Vanin, A.F. (1989). Similar endothelium-independent arterial relaxation by carbon monoxide and nitric oxide. Biomed. Biochim. Acta 48 601-3. 

Anderson, D.E., Yuan, X.J., Tseng, C.M. et al. (1993). Nitrone spin traps block calcium channels and induce pulmonary artery relaxation independent of free radicals. Biochem. Biophys. Res. Commun. 193 878-85. 

Gruetter, C., Barry, BK, McNamara, DB, Kadowitz, PJ, and Ignarro, LJ. 1980. Coronary arterial relaxation and guanylate cyclase activation by cigarette smoke, N -nitrosonomicotine and nitric oxide. J Pharmacol Exp Ther 214 9-15. 

Some /i-blockers may also interfere with the NO-pathway. For example, nebivolol, a /31-blocker and a racemic mixture of (S,R,R,R) and (R,S,S,S) enantiomers (88, 95), was found to induce endothelium-dependent arterial relaxation in dogs in a dose-dependent fashion (96). However, its hemodynamic effects differ from those of classical -adrenoceptor antagonists as a result of a vasodilating action. Indeed, the endothelium-dependent relaxation induced by nebivolol is abolished by L-NAME, an inhibitor of NOS. 

Burke TM and Wolin MS Hydrogen Peroxide Elicits Pulmonary Artery Relaxation and Guanylate Cyclase Activation. Am. J. Physiol. 1987 252(4 Pt 2) H721-32. 

Celermajer, D. S., Cullen, S., and Deanfieid, J. E. (1993). Impairment of endothelium-dependent pulmonary artery relaxation in children with congenital heart disease and abnormal pulmonary hemodynamcis. Circulation 87, 440-446. 

Dinh-Xuan, A. T., Higenbottam, T. W., Clelland, C. A., et al. (1991). Impairment of endothelium-dependent pulmonary-artery relaxation in chronic obstructive lung disease. N. Engl. J. Med. 324, 1539-1547. 

Inoue T, Saniabadi AR, Matsunaga R, et al. Impaired endothelium-dependent acetylcholine-induced coronary artery relaxation in patients with high serum remnant lipoprotein particles. Atherosclerosis 1998 139 363-367. 

Franco-Obregon A, Urena J, Lopez-Bameo J. Oxygen-sensitive calcium channels in vascular smooth muscle and their possible role in hypoxic arterial relaxation. Proc Natl Acad Sci USA 1995 92 4715-4719. 

Burke TM, Wolin MS. Hydrogen peroxide elicits pulmonary arterial relaxation and guanylate cyclase activation. Am J Physiol 1987 252 H721-H732. 

Burke-Wolin TM, Wolin MS. Inhibition of cGMP-associated pulmonary arterial relaxation to H2O2 and O2 by ethanol. Am J Physiol 1990 258 H1267-H1273. 

Gupte SA, Rupawalla T, Phillibert D Jr, Wolin MS. NADPH and heme redox modulate pulmonary artery relaxation and guanylate cyclase activation by NO. Am J Physiol 1999 277 L1124-L1132. 

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