Acts with the cardiovagal centre to maintain B.P. (Ref Ganong 23/e p556]Neural regulation of the blood pressure is brought about by 2 different centres located in medulla - Vasomotor centre which control the sympathetic outflow, and Cardiovagal centre which controls the parasympathetic outflow.TheVasomotor centre and the Cardiovagal centre act together to maintain the B.P. (Note that many books do not make the distinction between the vasomotor and cardiovagal centre and collectively use the term vasomotor centre for all the neurons in medulla that control the B.P.Vasomotor centreCardio vagal centreVasomotor centre is group of neurons located in RostralCardiovagal centre lies in the nucleus ambiguous.Ventrolateral Medulla (RVLM) associated with sympatheticIt sends parasympathetic impulses to the hea thedischarge controlling the cardiovascular system.vagus(note that blood vessels receive onlyThe sympathetic discharge from vasomotor centre goes tosympathetic impulses whereas hea receives bothhea and blood vessels resulting in:sympathetic and parasympathetic supply).- Increased hea rate (Chronotropic effect)This results in:- Increased force of cardiac contraction (Inotropic effect)- Decreased hea rate- Increased rate of transmission in the cardiac conductive- Decrease cardiac outputtissue (Dromotropic effect)- Decreased B.P.- Vasoconstriction(this leads to increased stroke volume and increased BP) The vasomotor centre receive inputs from Coicohypothalmic fibres Coicohypothalmic .fibres are descending tracts to the vasomotor area from the cerebral coex (paicularly the limbic coex) that relay in the hypothalamus. These fibers are responsible .for the blood pressure rise and tachycardia produced by emotions such as sexual excitement and anger.The vasomotor centre is not silent during sleep The vasomotor centre neurons arc tonically active and discharge rhythmically.The vasomotor centre receives inputs from baroreceptors and also from chemoreceptors.The baroreceptors are stretch receptors in the walls of carotid sinus and aoic arch. The baroreceptors are stimulated by distention of the structures in which they are located, and so they discharge at an increased rate when the pressure in these structures rises. Increased baroreceptor discharge inhibits the tonic discharge of sympathetic nerves and excites the vagal innervation of the hea. These neural changes produce vasodilation, venodilation, a drop in blood pressure. bradycardia, and a decrease in cardiac output.Chemoreceptors are located in carotid and aoic bodies. These receptors are primarily activated by a reduction in paial pressure of oxygen (Pa02), but they also respond to an increase in the paial pressure of carbon dioxide (PaCO2) and pH. Chemoreceptors exe their main effects on respiration; however, their activation also leads to vasoconstriction. Hea rate changes are variable and depend on various factors, including changes in respiration.Factors Affecting the Vasomotor centre (RVLM)Direct stimulationCO2HypoxiaExcitatory inputsCoex hypothalamusMesencephalic periaqueductal grayBrain stein reticular formationPain pathwaysSomatic afferents (somatosympathetic reflex)Carotid and aoic chemoreceptorsInhibitory inputsCoex hypothalamusCaudal ventrolateral medullaCaudal medullary raphe nucleiLung inflation afferentsCarotid, aoic, and cardiopulmonary baroreceptorsThus we see that the cardiovascular system is under neural influences of medulla, which in turn receive feedback from sensory receptors in the vasculature (eg, baroreceptors). An increase in neural output from the brain stem to sympathetic nerves leads to a decrease in blood vessel diameter (aeriolar constriction) and increases in stroke volume and hea rate, which contribute to a rise in blood pressure. This in turn causes an increase in baroreceptor activity, which signals the vasomotor centre to reduce the neural output to sympathetic nerves.Also know:The neurons of vasomotor centre secrete excitatory transmitter- glutamate (and not epinephrine)Inflation of the lungs causes vasodilation and a decrease in blood pressure. This response is mediated vagal afferents from the lungs that inhibit vasomotor discharge.In general, stimuli that increase the hea rate also increase blood pressure, whereas those that decrease the hea rate lower blood pressure. However, there are exceptions, such as the production of hypotension and tachycardia by stimulation of atrial stretch receptors and the production of hypeension and bradycardia by increased intracranial pressure (Cushing reflex).Cushing reflex: Increase in intracranial pressure compromises the blood supply to the vasomotor neurons, and the resulting local hypoxia and hypercapnia increase discharge from the vasomotor centre. This results in rise in systemic aerial pressure (Cushing reflex) which tends to restore the blood flow to the medulla. Over a considerable range, the blood pressure rise is propoional to the increase in intracranial pressure. The rise in blood pressure causes a reflex decrease in hea rate the aerial baroreceptors. This is why bradycardia rather than tachycardia is characteristically seen in patients with increased intracranial pressure.