Muscle, stress control

MR are present in, e.g. the central nervous system (CNS, for respiratory and cardiovascular activity, cognition and stress processing), peripheral nervous system (PNS, for smooth muscle contraction, control of heart rate, vasodilatation), as well as the sympathetic and parasympathetic ganglion cells [1], Five metabotropic cholinergic MR subtypes (M1-M5) were identified [1], but selectivity of TA is merely apparent [9] except for tiotropium and ipratropium [31]. 

The lime course of changes in high-energy phosphates (HEPs) (ATP and PCr) and their metabolites in skeletal muscles of control rats and those acutely intoxicated with carbofuran (l.Smg/kg, sc) (Table 3) revealed that in controls the levels of ATP and PCr are higher in the EDL than in the soleus. At the time of maximal severity (i.e., 1 hr after carbofuran expo.sure), the levels of ATP, total adenine nucleotides (TAN = ATP + ADP + AMP), NAD, PCr, and total creatine compounds (TCC = PCr + Cr) were maximally reduced in both muscles. Slow recovery was seen after 2 or 3 hr, with complete recovery to control levels by 24 hr. The carbofuran-induced muscle hyperactivity increased mu,scle levels of p2-IsoPs and NO and reduced levels of HEPs and their metabolites and thus seemed to produce a rapid omset of oxidative Stress. 

The function of adrenaline is to mobilise all fuels that can be used by muscle to provide ATP to support physical activity in response to stress (i.e. fight or flight response). And to increase sensitivity of regulation of enzymes involved in control of the rate of processes that generate ATP. The biochemical effects in the heart increase cardiac output, in preparation for fight or flight . 

Arteriolar and venous tone (smooth muscle tension) both play a role in determining myocardial wall stress (Table 12-1). Arteriolar tone directly controls peripheral vascular resistance and thus arterial blood pressure. In systole, intraventricular pressure must exceed aortic pressure to eject blood arterial blood pressure thus determines the systolic wall stress in an important way. Venous tone determines the capacity of the venous circulation and controls the amount of blood sequestered in the venous system versus the amount returned to the heart. Venous tone thereby determines the diastolic wall stress. 

The nitrates act by releasing nitric oxide, which relaxes vascular smooth muscle. The discovery that endothelium-derived relaxing factor (EDRF) is nitric oxide (1) stimulated new interest in these drugs, as nitric oxide not only controls local vessel wall tension in response to shear stress, but also plays a role in regulating the interaction of platelets with blood vessel walls. The release of nitric oxide from the walls of atheromatous arteries is reduced, because of malfunctioning or absent endothelium. Atheromatous arteries behave differently from healthy arteries, in that these vessels vasoconstrict rather than vasodilate when stimulated by acetylcholine. This impairment of the acetylcholine vasomotor response appears to be related to serum cholesterol concentration (2). 

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