Regulation Of Systemic Arterial Pressure

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Integration of Cardiovascular Function

Regulation of Systemic Arterial Pressure



Neural regulation



Humoral regulation



Autoregulation



Long term and short term regulation of BP

 Neural Regulation

a. Heart: sympathetic and parasympathetic nerves

The sympathetic and parasympathetic nerves to the heart, many of which closely accompany each other in and through the various cardiac and coronary plexuses.

Sympathetic

Contraction ↑ Conduction ↑ Heart rate ↑

Parasympathetic

Contraction ↓ Conduction ↓ Heart rate ↓

b. Cadiovascular Center The neuron groups or collection located central nervous system response to integrate cardiac activity and vasomotor.

 Medulla— basic center, a source of tonic activity for cardiovascular system.

c. Cardiovascular Reflexes Baroreceptor reflex

Sensors The carotid sinus Swellings in internal carotid artery wall Glossopharyngeal nerve to cardiovascular center in medulla Maintains normal BP in the brain

The aortic arch Receptors in wall of ascending aorta Vagus nerve to cardiovascular center Maintains general systemic BP

Control  Afferent signals transmitted from the pressoreceptors by sensory nerves to the medullary cardiovascular centers in the brain stem.  Efferent signals divide into two pathways: o Parasympathetic via the vagus nerve o Sympathetic nerves to the heart and peripheral vasculature.

Blood pressure rises Baroreceptors Vagus nerve

summary

Vascular center Sympathetic nerve

Vagus nerve

Heart Contract

↓ , rate ↓

conduct



Blood pressure decrease

 Humoral Regulation

a. Epinephrine & Norepinephrine Source:



Adrenal gland

• sympathetic terminals. Binding receptors:

∀α & β

Circulating Epinephrine Causes:  Increased heart rate        



1

adrenoreceptor mediated)

 Vasoconstriction in most systemic arteries and veins ( α adrenoreceptors)  Vasodilatation in muscle and liver vasculatures (β 2-adrenoceptor)

Circulating Norepinephrine Causes:

 Increased heart rate (β

1

adrenoreceptor mediated)

 Vasoconstriction occurs (α adrenoreceptors )

b. Renin-angiotensin-aldosterone System

Renin Angiotensin Aldosterone

Functions of Angiotensin Constricts resistance vessels Acts upon the adrenal cortex to release aldosterone, which in turn acts upon the kidneys to increase H2O & Na+ reabsorption.

Stimulates the release of vasopressin (antidiuretic hormone, ADH) from the posterior pituitary which acts upon the kidneys to increase fluid retention.

 Short Term Regulation

1. The baroreflex provides a mechanism for second-to-second homeostatic regulation of MAP, by bringing about instantaneous autonomic-mediated reflex adjustments in CO to restore normal MAP. 2. However, the baroreflex is inefficient in long-term (minutes-days) regulation of MAP, because the baroceptors adapt rapidly to prolonged changes in MAP which changes the set point for baroreceptor response.

 Long Term Regulation

1. In the lomg-term, maintenance of MAP is totally dependent on maintenance of constant blood volume by the kidneys. Blood volume is a major determinant of arterial blood pressure because it influences venous return and, consequently CO.

2. This an increase in blood volume leads to increased venous return which results in increased CO and MAP. When blood volume increases, the consequent increase in MAP leads to increased filtration of blood by the kidneys, which results in increased urinary excretion of sodium and water, thereby reducing plasma volume and MAP. Thus there is a reciprocal relationship between MAP and blood volume.

Overall Blood Pressure Regulation

Short-term regulation (seconds to minutes)  baroreceptors lead to changes in sympathetic & parasympathetic tone

Long-term regulation (hours to days) largely a function of the kidneys and elements of the endocrine system with both CNS-dependent and independent inputs that reset the baseline blood pressure, around which the short-term regulatory mechanisms still operate to defend.

Thank you!

Diseases/conditions Are Associated With Endothelial Dysfunction and Reduced NO Production And/or bioavailability 

Hypertension



Obesity



Diabetes



Heart failure



Atherosclerosis

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