Cardiovascular baroreceptors

Immunohistochemistry studies have shown that the NTS contains a rich innervation of substance P immunoreactive nerve terminals arising from cardiovascular, baroreceptor, and chemoreceptor afferent nerves, bronchopulmonary afferent... 

Cardiovascular-peripheral vasodilation,decreased peripheral resistance, inhibition of baroreceptors (pressure receptors located in the aortic arch and carotid sinus that regulate blood pressure), orthostatic hypotension and fainting... 

An example of this type of reflex is the baroreceptor reflex (see Figure 1.2). Baroreceptors located in some of the major systemic arteries are sensory receptors that monitor blood pressure. If blood pressure decreases, the number of sensory impulses sent from the baroreceptors to the cardiovascular control center in the brainstem also decreases. As a result of this change in baroreceptor stimulation and sensory input to the brainstem, ANS discharge to the heart and blood vessels is adjusted to increase heart rate and vascular resistance so that blood pressure increases to its normal value. 

Figure 15.4 Effects of the autonomic nervous system on mean arterial pressure. The baroreceptors, chemoreceptors, and low-pressure receptors provide neural input to the vasomotor center in the brainstem. The vasomotor center integrates this input and determines the degree of discharge by the sympathetic and parasympathetic nervous systems to the cardiovascular system. Cardiac output and total peripheral resistance are adjusted so as to maintain mean arterial pressure within the normal range.

Cardiovascular 1 Myocardial sensitivity to /J-adrenergic stimulation 1 Baroreceptor activity i Cardiac output T Total peripheral resistance... 

Many other changes make older adults more vulnerable regarding cardiovascular drugs. There is a decrease in baroreceptor reflex response. This may explain the increased sensitivity to nitrates (Marchionni et al. 1990). With age there is a loss of blood vessel distensibility and enhanced intimal thickness. This can partly explain the increase of systolic blood pressure. Aging is also associated with a reduction in baroreflex-mediated heart rate response to hypotensive stimuli (Verhaeverbeke and Mets 1997, Lakatta and Levy 2003). 

The injection of a vasoconstrictor, which causes an increase in mean arterial blood pressure, results in activation of the baroreceptors and increased neural input to the cardiovascular centers in the medulla oblongata. The reflex compensation for the drug-induced hypertension includes an increase in parasympathetic nerve activity and a decrease in sympathetic nerve activity. This combined alteration in neural firing reduces cardiac rate and force and the tone of vascular smooth muscle. As a consequence of the altered neural control of both the heart and the blood vessels, the rise in blood pressure induced by the drug is opposed and blunted. 

The net effect of norepinephrine administration on heart rate and ventricular contractile force therefore varies with the dose of norepinephrine, the physical activity of the subject, any prior cardiovascular and baroreceptor pathology, and the presence of other drugs that may alter reflexes. 

Clonidine (4.42) is an ttj agonist. Therapeutically, clonidine is a central antihypertensive agent, which may perhaps act on the baroreceptor (blood pressure sensor) reflex pathway, on cardiovascular centers in the medulla, and also peripherally. As is evident... 

Reflex arcs Most of the afferent impulses are translated into reflex responses without involving consciousness. For example, a fall in blood pressure causes pressure-sensitive neurons (baroreceptors in the heart, vena cava, aortic arch, and carotid sinuses) to send fewer impulses to cardiovascular centers in the brain. This prompts a reflex response of increased sympathetic output to the heart and vasculature, and decreased parasympathetic output to the heart, which results in a compensatory rise in blood pressure and tachycardia (see Figure 3.5). 

The short-term mechanism controlling BP from minute to minute involves arterial baroreceptors. When changing body position, baroreceptors detect changes in BP and elicit reflex responses via the cardiovascular centre in the medulla, which reverse the change and return BP to the original level. Baroreceptors operate these reflexes in hypertension, but adapt to the increased pressure so that they operate around a higher set point. 

The opioids are considered relahvely safe from a cardiovascular standpoint. Myocardial depression is minimal. Changes in heart rate are species dependent and usually manifest as a mild decrease in heart rate however, a significant increase in heart rate can be seen in horses, which is consistent with the central excitatory effect that often occurs. Opioids inhibit the baroreceptor reflex response to changes in blood pressure. Certain opioids may cause systemic vasodilatation, decreased peripheral vascular resistance and hypotension secondary to histamine release. Morphine and meperidine (pethidine) are the opioids most likely associated with this effect. This is typically seen after rapid i.v. administration, is dose dependent and does not result from mast cell... 

Barbiturates are associated with dose-dependent cardiovascular depression. However, because of preservation of the baroreceptor reflex, the hemo-d3mamic response to an induction dose of thiopental is mild. Heart rate generally increases to compensate for a brief fall in arterial blood pressure. As a result of this reflex response, blood pressure remains unchanged and cardiac output may increase slightly with the elevation in heart rate (Ilkiw et al 1991). Without the compensatory heart rate response, or if the change in heart rate is small, a decrease in systemic blood pressure and cardiac output would predominate. 

Cardiovascular 4 Myocardial sensitivity to beta-adrenergic stimulation 4 Baroreceptor activity 4 Cardiac output t Total peripheral resistance... 

Blood pressure is the product of total peripheral resistance (TPR) and cardiac output (CO). Both branches of the ANS are involved in the autonomic (or neural) control of blood pressure via feedback mechanisms. Changes in mean blood pressure are detected by baroreceptors, which relay information to the cardiovascular centers in the brainstem controlling PANS and SANS outflow. For example, an increase in mean blood pressure elicits baroreceptor discharge,... 

Blood pressure (BP) is a product of the total peripheral resistance (TPR) times the cardiac output (CO). The CO is equal to the heart rate (HR) times the stroke volume (SV). The autonomic (neural) system helps regulate the BP through feedback control involving the baroreceptors, the cardiovascular centers in the brain stem, and the PANS and SANS, which act in an opposing but coordinated manner to regulate the pressure. 

Grundemar, L., Wahlestedt, C. Reis, D.J. (1991a) Long-lasting inhibition of the cardiovascular responses to glutamate and the baroreceptor reflex elicited by neuropeptide Y injected into the nucleus tractus solitarius. Neurosci. Lett. 122, 135-139. 

The arterial blood pressure within the mammalian organism, whether normal or abnormal, is ultimately determined by cardiac output and peripheral resistance to flow. Of the several physical and chemical variables of the cardiovascular system, blood pressure is ordinarily the most constant. This is especially remarkable if one considers the large variations encountered in cardiac output and in heart rate. This feat is accomplished by a negative feedback system. The chief mechanism involves the baroreceptor reflex. 

Baroreceptors are stretch receptors in the arterial portion of the cardiovascular system, specifically in the carotid region and in the aortic arch. They monitor (sense) hydrostatic pressure through specialized nerve endings that are sensitive to mechanical deformation of the blood vessel wall. Nerve impulses over these afferent fibers to the central nervous system increase whenever the arterial pressure in the vicinity of the baroreceptors increases. This inhibits outflow of sympathetic impulses, reducing vasomotor tone and decreasing the heart rate. Thus vasoconstrictor tone and cardiac output are reduced as a result of the initial pressure increase that caused these series of events to occur. Both factors tend to return the pressure to previous, lower levels. 

Receptors for angiotensin II are found in the medulla oblongata in neurons involved in the regulation of barore-ceptor activity. Because studies in hypertensive patients have indicated that ACE inhibitors reduce sympathetic activity and enhance baroreceptor sensitivity, it is possible that the primary hypotensive mechanism of these agents is mediated through the blockade of angiotensin II formation in the cardiovascular centers of the brain. 

CARDIOVASCULAR SYSTEM ACh has four primary effects on the cardiovascular system vasodilation, a decrease in cardiac rate (the negative chronotropic effect), a decrease in the rate of conduction in the specialized tissues of the SA and atrioventricular (AV) nodes (the negative dromotropic effect), and a decrease in the force of cardiac contraction (the negative inotropic effect). The last effect is of lesser significance in ventricular than in atrial muscle. Certain of the above responses can be obscured by baroreceptor and other reflexes that dampen or counteract the direct responses to ACh. 

Cardiovascular The anesthetic barbiturates produce dose-dependent decreases in blood pressure that are due primarily to vasodilation, particularly venodUation, and to a lesser degree to a direct decrease in cardiac contractility. Typically, heart rate increases as a compensatory response to a lower blood pressure, although barbiturates also blunt the baroreceptor reflex. 

Cardiovascular Propofol produces a dose-dependent decrease in blood pressure that is significantly greater than that produced by thiopental the effect is explained by vasodilation and mild depression of myocardial contractility. Propofol appears to blunt the baroreceptor refiex or is directly vagotonic. As with thiopental, propofol should be used with caution in patients at risk for or intolerant of decreases in blood pressure. 

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