CARDIOVASCULAR PHYSIOLOGY BLOOD PRESSURE AND ITS REGULATION

At the end of this lecture you should be able to OBJECTIVES At the end of this lecture you should be able to Define blood pressure and Mean Arterial Pressure (MAP) List the factors affecting MAP Describe Short term and long term control of Blood Pressure

BLOOD PRESSURE REGULATING MECHANISMS Short Term (Nervous System works within few seconds) Baroreceptors Chemoreceptors CNS Ischemic Response Long Term (Renal Control works within few days) Intermediate (Within few hours) Stress relaxation Capillary fluid shift

VASOMOTOR CENTER (Area!) 1. Vasoconstrictor area 2. Vasodilator area 3. Sensory area

VASOMOTOR CENTER (Area!) 1. A vasoconstrictor area located bilaterally in upper medulla. excite vasoconstrictor neurons of the sympathetic nervous system. 2. A vasodilator area located bilaterally in the lower half of the medulla. inhibit the vasoconstrictor area, thus causing vasodilation. 3. A sensory area located bilaterally in medulla and pons (tractus solitarius). Receive sensory nerve signals from vagus and glossopharyngeal nerves and output control the vasoconstrictor and vasodilator areas An example is the baroreceptor reflex Nervous Regulation of Circulation The Autonomic Nervous System Sympathetic Vasoconstrictor Tone (Vasomotor Tone) Control of Vasomotor Center Baroreceptor Control System

in most tissues all the vessels except the capillaries, precapillary sphincters, and metarterioles are innervated. Continuous Partial Constriction of the Blood Vessels Is Normally Caused by Sympathetic Vasoconstrictor Tone.

CONTROL OF VMC Reticular Substance of Brain Stem Hypothalamus Posterolateral portions Cause Excitation. Anterior part can cause Excitation or Inhibition Cerebral Cortex Motor Cortex Cause Excitation

Control of blood pressure Short-term Control Long-term control Baroreceptor reflex Renal compensation

Baroreceptors

Baroreceptor Reflex Mediated Quick operation through (within few autonomic nerves Quick operation (within few seconds) Influences heart & blood vessels Adjusts CO &TPR to restore BP to normal

Renal Control It is perfect 100 % Mediated through Kidneys Renin Angiotensin aldosterone mechanism, Slow operation (within hours to Days) Adjusts urinary output and TPR to restore BP to normal Influences Kidneys & blood vessels

Components Of Baroreceptor Reflex Arc Receptors Baroreceptors in carotid sinuses & arch of aorta Afferents Carotid sinus nerves & nerve from arch of aorta Center Vasomotor Center in medulla oblongata Efferents Sympathetic & parasympathetic nerves Effectors Heart and blood vessels Carotid sinus nerve runs along with glossopharyngeal nerve Aortic nerve runs along with vagus nerve

BARORECEPTOR REFLEX ARC COMPONENTS OF BARORECEPTOR REFLEX ARC

Vasomotor Center in medulla oblongata Heart and blood vessels Stimulus Increase in BP Receptors Baroreceptors Increase Firing of Glossopharyngeal and Vagus Nerves Afferents Vasomotor Center in medulla oblongata Center  Sympathetic &  parasympathetic firing Efferents Heart and blood vessels Effectors Heart rate and force of contraction and Vasodilatation  BP Effects

Stimulus Receptors Afferents Center Efferents Effectors Effects Decrease in BP Receptors Baroreceptors Minimal Firing of Glossopharyngeal and Vagus Nerves Afferents Vasomotor Center in medulla oblongata Center  Sympathetic &  parasympathetic firing Efferents Heart and blood vessels Effectors Heart rate and force of contraction and Vasoconstriction  BP Effects

Baroreceptor reflex Baroreceptor reflex  MAP  Firing of baroreceptors  Sympathetic tone  Vagal tone Vasodilatation  HR  SV  TPR  Cardiac output  MAP

? ? !! OR Can you guess ! Because the inhibitory What shall be the effect of bilateral clamping of the carotid arteries proximal to the carotid sinuses? ? OR Rise in blood pressure and heart rate. Because the inhibitory control of sympathetic is gone Can you guess ! What shall be the effect of bilateral cutting of the carotid sinus nerves? ? !!

Pressure on the carotid sinus, produced, for example by the tight collar or carotid massage can cause marked bradycardia vasodilatation Fainting or syncope

Transient loss of consciousness Syncope Transient loss of consciousness Associated with Abrupt vasodilatation Inadequate cerebral blood flow Hypotension and bradycardia

Pressure “Buffer” Function of the Baroreceptor Control System.

Pressure “Buffer” Function of the Baroreceptor Control System.

COTROL OF ARTERIAL PRESSURE IS ALSO BY Chemoreceptors (Carotid and Aortic Bodies) Atrial and Pulmonary Artery Reflexes (Low Pressure Receptors) CNS Ischemic Response

Pressure Natriuresis and Pressure Diuresis

Two ways in which the arterial pressure can be increased: A, by shifting the renal output curve in the right-hand direction toward a higher pressure level or B, by increasing the intake level of salt and water.

Increased Fluid Volume Can Elevate Arterial Pressure by Increasing Cardiac Output or Total Peripheral Resistance

Salt (NaCl) intake & Arterial Pressure Regulation

Renal control  MAP  Renin secretion Angiotensinogen Angiotensin I ACE in Lungs Angiotensin II Vasoconstriction Salt & water Retention  TPR  ECF Volume  MAP

ACE synthesize Ang II (Vascoconstrictor) and Inactivates Bradykinin (Vasodilator) Two related vasodilator peptides called kinins are found in the body. One is the nonapeptide bradykinin, and the other is the decapeptide lysylbradykinin, also known as kallidin (Figure 33–11). Lysylbradykinin can be converted to bradykinin by aminopeptidase. Both peptides are metabolized to inactive fragments by kininase I, a carboxypeptidase that removes the carboxyl terminal arginine (Arg). In addition, the dipeptidylcarboxypeptidase kininase II inactivates bradykinin and lysylbradykinin by removing phenylalanine-arginine (Phe-Arg) from the carboxyl terminal. Kininase II is the same enzyme as angiotensin-converting enzyme (see Chapter 39), which removes histidine-leucine (His-Leu) from the carboxyl terminal end of angiotensin I.

Renal control of blood presure  MAP  MAP Renal control of blood presure  Urine formation  Cardiac output  Blood volume  Stroke volume  venous return  EDV

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