Vasoconstrictor Agents Norepinephrine and Epinephrine Norepinephrine is an especially powerful vasoconstrictor hormone; epinephrine is less so When the sympathetic nervous system is stimulated, the sympathetic nerve endings in the individual tissues release norepinephrine, which excites the heart and contracts the veins and arterioles In addition, the sympathetic nerves to the adrenal medullae cause these glands to secrete both norepinephrine and epinephrine into the blood
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Vasoconstrictor Agents
Norepinephrine and Epinephrine Norepinephrine is an especially powerful
vasoconstrictor hormone; epinephrine is less so When the sympathetic nervous system is
stimulated, the sympathetic nerve endings in the individual tissues release norepinephrine, which excites the heart and contracts the veins and arterioles
In addition, the sympathetic nerves to the adrenal medullae cause these glands to secrete both norepinephrine and epinephrine into the blood
Angiotensin II
Angiotensin II is powerful vasoconstrictor substance
The effect of angiotensin II is to constrict powerfully the small arterioles and decreases the blood flow
Angiotensin II increases the total peripheral resistance, thereby increasing the arterial pressure
Vasopressin
Vasopressin, also called antidiuretic hormone, one of the body's most potent vascular constrictor substances
The concentration of circulating blood vasopressin after severe hemorrhage can rise high enough to increase the arterial pressure
In many instances this canbring the arterial pressure almost back up to normal
Other chemical influences on blood flow
Histamine
Most of the histamine is derived from mast cells in the damaged tissues
Histamine has a powerful vasodilator
Has the ability to increase greatly capillary porosity, allowing leakage of both fluid and plasma protein into the tissues
Bradykinin
Bradykinin causes both powerful arteriolar dilation and increased capillary permeability
Bradykinin play special roles in regulating blood flow and capillary leakage of fluids in inflamed tissues
Vascular Control by Ions and Other Chemical Factors
1. An increase in calcium ion concentration causes vasoconstriction
2. An increase in potassium ion concentration causes vasodilation
3. An increase in magnesium ionconcentration causes powerful vasodilation
4. An increase in hydrogen ion concentration causes dilation of the arterioles
5. An increase in carbon dioxide concentrationcauses moderate vasodilation in most tissues, but marked vasodilation in the brain
Vascular Control by Ions and Other Chemical Factors
Pharmacologic Stimuli that Cause Contraction or Relaxation of Vascular Smooth Muscle
Vasoconstrictors Norepinephrine and
epinephrine Endothelin Angiotensin II Vasopressin Calcium
Skeletal muscles are provided with sympathetic vasoconstrictor nerves
Sympathetic vasoconstrictor secrete norepinephrine in their nerve ending (important during shock and stress)
Epinephrine – secreted by adrenal medullae gives vasodilator effect during exercise
Total Body Circulatory Readjustments During Exercise
Three major effects occur during exercise
(1) mass discharge of the sympathetic nervous system throughout the body
(2) increase in arterial pressure
(3) increase in cardiac output
Effects of Mass Sympathetic Discharge
Three major circulatory effects result
1. The heart is stimulated to greatly increased heart rate and increased pumping strengthas a result of the sympathetic drive to the heart plus release of the heart from normal parasympathetic inhibition
Effects of Mass Sympathetic Discharge
2. Most of the arterioles of the peripheral circulation are strongly contracted, except for the arterioles in the active muscles, which are strongly vasodilated by the local vasodilator
Two of the peripheral circulatory systems, the coronary and cerebral systems, are spared this vasoconstrictor effect
3. The muscle walls of the veins are contracted powerfully, which greatly increases the mean systemic filling pressure
This is one of the most important factors in promoting increase in venous return of blood to the heart and, therefore, in increasing the cardiac output