Regulation of circulation and blood pressure overview

Regulation of circulation and BP Nervous control Renal-body fluid system Renin-angiotensin Aldosterone ADH

OUTLINE OF NERVOUS CONTROL OF CVS

Nervous control is through Autonomic Nervous System (ANS) ANS has two parts Sympathetic (mainly controls blood vessels) Parasympathetic (mainly controls heart)

Physiologic anatomy of sympathetic system Sympathetic vasomotor nerve fibers leave the spinal cord through all the thoracic spinal nerves and through the first one or two lumbar spinal nerves. They then pass immediately into a sympathetic chain, one of which lies on each side of the vertebral column. Next, they pass by two routes to the circulation: (1) through specific sympathetic nerves that innervate mainly the vasculature of the internal viscera and the heart, (2) almost immediately into peripheral portions of the spinal nerves distributed to the vasculature of the peripheral areas

Sympathetic innervation of blood vessels All vessels except capillaries are innervated Very little innervation of metarterioles and precapillary sphincters Rich innervation of arterioles, small arteries Innervation of veins Innervation of heart

Effect of sympathetic stimulation Increased heart rate Increased force of contraction Constriction of arterioles Constriction of veins Increased release of adrenaline by adrenal medulla Increased renin release by kidneys

Neurotransmitter of sympathetic nerve endings at most areas is noradrenaline Adrenal medulla produces adrenaline and nor adrenaline

In skeletal blood vessels Nor epinephrine causes vasoconstriction Epinephrine causes vasodilation Metabolic control is the most effective way

Parasympathetic innervation It is through vagus nerve to heart It decreases heart rate Slightly decreases contractility of heart

Vasomotor area Vasomotor area is located in lower pons and medulla bilaterally It sends parasympathetic impulses to heart through vagus It sends sympathetic impulses through spinal cord

Important parts of vasomotor center Vasoconstrictor area located bilaterally in anterolateral part of upper medulla Vasodilator area located bilaterally in anterolateral part of lower medulla Sensory area called Tractus solitarius located bilaterally in posterlateral part of medulla and lower pons

Control of heart by vasomotor center Lateral part increases heart rate Medial part decreases heart rate through vagus

Control of vasomotor center by higher centers of CNS Hypothalamus (Posterior part is excitatory, anterior is inhibitory) Reticular substance of pons, midbrain, diencephalon Limbic system Motor areas of cerebral cortex

Vasomotor tone In resting state vasoconstrictor area of vasomotor center sends excitatory signals to spinal cord Which sends excitatory signals to blood vessels These impulses maintain baseline contraction of smooth muscles of blood vessels This baseline sympathetic discharge maintaining smooth muscle contraction of blood vessels is called vasomotor tone

Vasovagal syncope Fainting due to disturbed emotional thoughts in cerebral cortex From cerebral cortex to anterior hypothalamus Stimulation of vagus nerve Activation of vasodilator sympathetic fibers of skeletal muscles Pooling of blood in vessels of muscles

Vasodilatation of skeletal vessels Fall in BP Decreased heart rate Brain is deprived of blood flow Person faints

Control of BP through nervous system How sympathetic system increases BP Constriction of arterioles Constriction of veins Stimulation of heart

Reflex mechanisms for maintaining BP Baroreceptor Chemoreceptors Low pressure receptors(volume reflex, Inc H.R) CNS ischemic response Abdominal compression reflex

Baroreceptor reflex

Components of baroreceptor reflex Afferent Center Efferent Effectors

Receptors Baroreceptors (Nerve endings) located in carotid sinus present in internal carotid artery Aortic arch Also present in few great vessels of neck and thorax These receptors are excited by stretch due to increase in BP (60-180)

Center Integration occurs at vasomotor center Sensory input is received at Tractus solitarius in medulla and lower pons From TS impulses go to vasoconstrictor area and to vagus nerve nucleus.

Efferents Vagus nerve resulting in slowing of heart Decreased activity of sympathetic nerves arising from vasomotor center resulting in less constriction of vessels and decreased cardiac activity Long term rise in BP also decreases sympathetic activity in kidneys

Effectors Heart Blood vessels kidneys

When person stands from lying position When a person goes from supine to an upright posture, the following important changes take place: Pressure in the dependent veins increases. Blood volume in the dependent veins increases. Circulating blood volume (cardiac output) decreases. Blood pressure decreases in upper half. Compensation via the carotid sinus reflex will include: Total peripheral resistance increases. Heart rate increases. The changes induced by the carotid sinus returns blood pressure toward the value in the supine position, but in cases compensation will not be complete.

Chemoreceptor reflex

Receptors Receptors are Chemoreceptors which are present in aortic bodies and carotid bodies (common carotid arteries) Stimulated by rise in H ions and CO2 , and fall in O2 Stimulated by BP below 80 mm of Hg

Afferents From carotid bodies impulses are conducted through Hering’s nerve to glossopharyngeal nerve to Tractus solitarius From aortic arch impulses are conducted through vagus nerve to tractus solitarius

Center and effectors Integration occurs at Vasomotor center and respiratory center If BP falls rise in BP by vaso-constriction Stimulation of respiratory center

Atrial reflexes Bainbridge reflex (control of heart rate) Stimulation of SA node (control of heart rate) Atrial volume reflexes that activate the kidneys (dilation of arterioles of kidneys and decreased secretion of ADH) Increased production of ANP

Bainbridge reflex This reflex is initiated when the nerve endings in the wall of the right atrium are stimulated by a rise of venous pressure. The afferent fibers ascend in the vagus to the medulla oblongata and terminate on the nucleus of the tractus solitarius . Connector neurons inhibit the parasympathetic nucleus (dorsal) of the vagus, and sympathetic fibers stimulate the cardiac activity.

CNS Ischemic response The arterial pressure elevation in response to cerebral ischemia is known as CNS ischemic response. (very powerful response) The response becomes significant when arterial pressure falls below 60 mm of mercury. Maximum stimulation occurs at pressure of 15 to 20 mm of mercury

There is decreased blood flow to Vasomotor area Build up of CO2, lactic acid and other acidic substances in vasomotor center Due to CNS ischemic response blood pressure can rise up to 250 mm of mercury.

Due to this response BP rises as a result of intense sympathetic vasoconstriction of peripheral vessels

Cushing reaction This is CNS ischemic response due to rise in CSF pressure around the brain in cranial vault Cushing reaction protects vital centers of the brain from loss of nutrition, when CSF pressure becomes more than the arterial BP

Abdominal compression reflex Contraction of abdominal muscles Compression of blood vessels Increased venous return

Effect of respiration on BP In inspiration systolic BP falls by 10 mm of mercury In deep breathing this fall is about 20 mm of mercury During inspiration Pulmonary veins retain blood due to negative intrathoracic pressure and venous return to left atrium decreases and left ventricular output falls

Kidney-body fluid mechanisms Direct method Pressure diuresis Pressure natriuresis This is regulated by increase or decrease in BP Intake of salt and water At BP of 50 no urine output, at 100 normal output, at 200, 6-8 times normal

When renal artery BP INCREASE Reduction in water and sodium resorption in proximal tubule Increased BP  --> Increased peritubular capillary pressure  --> Increased renal interstitial pressure  --> Decreased fluid and sodium absorption Angiotensin II and sympathetic activity When BP increase, both angiotensin II and sympathetic activities decrease. Direct little increase in GFR

Control through renin angiotensin system

Actions of angiotensin 11 Acts directly on kidneys Causes release of Aldosterone Causes vasoconstriction Increases thirst

Components of renin-angiotensin system Renin stored as prorenin in JG cells of kidneys JG cells are smooth muscle cells of afferent arterioles Fall in BP causes release of renin from JG cells Renin converts angiotensinogen to angiotensin1 Angiotensin 1 is converted to angiotensin11 predominantly in the lungs by ACE

Renin-Angiotensin system is an effective feedback mechanism for regulating blood pressure

How increased salt intake is balanced in healthy subjects

Nervous mechsnisms, diuresis through kidneys and Renin-Angiotensin system if functioning properly are efficient mechanisms for preventing sudden change in BP If mechanisms are proper (Salt insensitive) If mechanisms not proper (Salt sensitive)

Regulation of blood pressure Rapidly Acting Pressure Control Mechanisms, Acting Within Seconds or Minutes Pressure Control Mechanisms That Act After Many Minutes Long-Term Mechanisms for Arterial Pressure Regulation.

Rapidly Acting Pressure Control Mechanisms, Acting Within Seconds or Minutes The Baroreceptor mechanism CNS ischemic response The Chemoreceptor mechanism

Pressure control mechanisms that act after many minutes These mechanisms start within 30 minutes to several hours Renin-angiotensin vasoconstrictor mechanism Stress relaxation of vasculature Fluid shift through capillary walls in and out of circulation

Long term mechanisms for arterial pressure regulation Secretion of Aldosterone Secretion of ADH