Baroreceptor reflex response

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 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... 

Shih, C.D., Chan, J.YH. Chan, S.H.H. (1992) Tonic supression of baroreceptor reflex response by endogenous neuropeptide Y at the nucleus tractus solitarius of the rat. Neurosci. Lett. 148, 169-172. 

List the determinants of blood pressure and describe the baroreceptor reflex response for the following perturbations (1) blood loss, (2) administration of a vasodilator, (3f a vasoconstrictor, (4) a cardiac stimulant, (5) a cardiac depressant. 

B. Bradycardia or atrioventricular block is common in patients with moderate to severe hypertension associated with PPA and phenylephrine, owing to the baroreceptor reflex response to hypertension. The presence of dmgs such as antihistamines or caffeine prevents reflex bradycardia and may enhance the hypertensive effects of PPA and phenylephrine. 

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. 

Loss of plasma volume leads to a decrease in MAP. Baroreceptors located in the aortic and carotid sinuses detect this fall in MAP and elicit reflex responses that include an increase in the overall activity of the sympathetic nervous system. Sympathetic stimulation of the heart and blood vessels leads to an increase in cardiac output (CO) and increased total peripheral resistance (TPR). These adjustments, which increase MAP, are responsible for the short-term regulation of blood pressure. Although increases in CO and TPR are effective in temporary maintenance of MAP and blood flow to the vital organs, these activities cannot persist indefinitely. Ultimately, plasma volume must be returned to normal (see Table 19.1). 

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. 

There is an excessive drop in BP during phase 2 with no associated overshoot in phase 4. There is no bradycardia in phase 4. The response is thought to be caused by a diminished baroreceptor reflex and so the normal compensatory changes in heart rate do not occur. 

In a normal resting subject who is receiving no drugs, there is a moderate parasympathetic tone to the heart, and sympathetic activity is relatively low. The ventricular muscle receives little, if any, parasympathetic innervation. As the blood pressure rises in response to norepinephrine, the baroreceptor reflex is activated, parasympathetic impulses (which are inhibitory) to the heart increase in frequency, and what little sympathetic outflow there is may be reduced. Heart rate is slowed so much that the direct effect of norepinephrine to increase the rate is masked and there is a net decrease in rate. Under the conditions described, however, the impact of the reflex on the ventricles is very slight because there is no parasympathetic innervation and the preexisting level of sympathetic activity is already low. A further decrease in sympathetic activity therefore would have little further effect on contractility in this subject. Thus, a decrease in heart rate and an increase in stroke volume will occur, and cardiac output will change very little. 

The administration of angiotensin II to an animal with intact baroreceptor reflexes results in reflex bradycardia in response to the marked vasoconstriction. When baroreceptor reflexes are depressed (barbiturate anesthesia) or if vagal tone is inhibited (atropine or vagotomy), angiotensin directly induces cardiac acceleration. 

There is no barorefiex-associated increase in heart rate, cardiac output, or myocardial contractility in response to the decrease in pressure, presumably because captopril decreases the sensitivity of the baroreceptor reflex. 

A slow intravenous injection of histamine produces marked vasodilation of the arterioles, capillaries, and venules. This causes a fall in blood pressure whose magnitude depends on the concentration of histamine injected, the degree of baroreceptor reflex compensation, and the extent of histamine-induced release of adrenal catecholamines. Vasodilation of cutaneous blood vessels reddens the skin of the face, while a throbbing headache can result from vasodilation of brain arterioles. Vasodilation is mediated through both Hj- and Hj-receptors on vascular smooth muscle. Stimulation of Hj-receptors produces a rapid and short-lived response, whereas stimulation of H2-receptors produces a more sustained response that is slower in onset. Stimulation of Hj-receptors on sympathetic nerve terminals inhibits the release of norepinephrine and its associated vasoconstriction. 

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... 

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. 

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. 

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. 

Drugs that affect the parasympathetic nervous system tend to produce a high degree of baroreceptor-mediated responses under normal usage. Thus, their responses are typically limited in duration, irrespective of drug half-life. This may not apply when the drug is used under life threatening conditions (e.g.. the use of atropine in the resuscitation of cardiac failure), because the baroreceptor reflex is set at normal levels of tension. 

The classical response of blood vessels to 5-HT is contraction, particularly in the splanchnic, renal, pulmonary, and cerebral vasculatures. This response also occurs in bronchial smooth muscle. 5-HT induces a variety of cardiac responses that result from activation of multiple 5-HT receptor subtypes, stimulation or inhibition of autonomic nerve activity, and reflex responses to 5-HT. Thus, 5-HT has positive inotropic and chronotropic actions on the heart that may be blunted by simultaneous stimulation of afferent nerves from baroreceptors and chemoreceptors. An effect... 

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. 

E. Toxicity of Nitrates and Nitrites The most common toxic effects of nitrates are the responses evoked by vasodilation. These include tachycardia (from the baroreceptor reflex), orthostatic hypotension (a direct extension of the venodilator effect), and throbbing headache from meningeal artery vasodilation. 

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