Vasomotor responses

Glonidine. Clonidine decreases blood pressure, heart rate, cardiac output, stroke volume, and total peripheral resistance. It activates central a2 adrenoceptors ia the brainstem vasomotor center and produces a prolonged hypotensive response. Clonidine, most efficaciously used concomitantly with a diuretic in long-term treatment, decreases renin and aldosterone secretion. 

Because baroreceptors respond to stretch or distension of the blood vessel walls, they are also referred to as stretch receptors. A change in blood pressure will elicit the baroreceptor reflex, which involves negative feedback responses that return blood pressure to normal (see Figure 15.6). For example, an increase in blood pressure causes distension of the aorta and carotid arteries, thus stimulating the baroreceptors. As a result, the number of afferent nerve impulses transmitted to the vasomotor center increases. The vasomotor center processes this information and adjusts the activity of the autonomic nervous system accordingly. Sympathetic stimulation of vascular smooth muscle and the heart is decreased and parasympathetic stimulation of the heart is increased. As a result, venous return, CO, and TPR decrease so that MAP is decreased back toward its normal value. 

A decrease in plasma volume leads to decreased MAP, which is detected by baroreceptors in the carotid sinuses and the arch of the aorta. By way of the vasomotor center, the baroreceptor reflex results in an overall increase in sympathetic nervous activity. This includes stimulation of the heart and vascular smooth muscle, which causes an increase in cardiac output and total peripheral resistance. These changes are responsible for the short-term regulation of blood pressure, which temporarily increases MAP toward normal. 

Kotlikojf These animals have an altered contractile response to agonists in vitro. This is about as much as we can say at the moment. We do see a phenotype in terms of their contractile properties. In the RyR2 knockouts we would expect to have a loss of stretch-induced Ca2+ release and CICR in smooth muscle. If you have normal pressurized vasomotor responses in those animals, I think this would suggest that the phenomenon that we have described is not essential for myogenic tone. 

Moderate to severe vasomotor symptoms associated with menopause - Initial dose is 0.3 mg daily. Subsequent dosage adjustment may be made based upon the individual patient response. 

Neurohumoral (extrinsic) compensation involves two major mechanisms (previously presented in Figure 6-7)—the sympathetic nervous system and the renin-angiotensin-aldosterone hormonal response—plus several others. Some of the pathologic as well as beneficial features of these compensatory responses are illustrated in Figure 13-2. The baroreceptor reflex appears to be reset, with a lower sensitivity to arterial pressure, in patients with heart failure. As a result, baroreceptor sensory input to the vasomotor center is reduced even at normal pressures sympathetic outflow is increased, and parasympathetic outflow is decreased. Increased sympathetic outflow causes tachycardia, increased cardiac contractility, and increased vascular tone. Vascular tone is further increased by angiotensin II and endothelin, a potent vasoconstrictor released by vascular endothelial cells. The result is a vicious cycle that is characteristic of heart failure (Figure 13-3). Vasoconstriction increases afterload, which further reduces ejection fraction and cardiac output. Neurohumoral antagonists and vasodilators... 

Fall in blood pressure with reflex tachycardia, vasomotor response... 

The mesencephalon, or midhrain, serves as a bridge between the higher areas of the brain (cerebrum and diencephalon) and the brainstem. The brainstem consists of the pons and the medulla oblongata. In addition to serving as a pathway between the higher brain and spinal cord, the midbrain and brainstem are the locations of centers responsible for controlling respiration and cardiovascular function (vasomotor center). 

Colchicine also exhibits a variety of other pharmacological effects. It lowers body temperature, increases the sensitivity to central depressants, depresses the respiratory center, enhances the response to sympathomimetic agents, constricts blood vessels, and induces hypertension by central vasomotor stimulation. It enhances gastrointestinal activity by neurogenic stimulation but depresses it by a direct effect, and alters neuromuscular function. 

Furthermore, some comorbidities seem to share potential genetic vulnerability factors with schizophrenia. An increased risk of myocardial infarction has been described in schizophrenia patients (Enger et al., 2004). Both GCLC and GCLM genes contain DNA polymorphisms which increase the susceptibility to coronary endothelial vasomotor dysfunction and myocardial infarction (Nakamura et al., 2002 Koide et al., 2003). The mutations associated with the myocardial infarction were described in promoter sequences of both GCL genes. It was shown that these alterations decreased the responsiveness to oxidative... 

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