Humoral control of the circulation means control by sub stances secreted or absorbed into the body fluids, such as hormones and locally produced factors. Some of these substances are formed by special glands and transported in the blood throughout the entire body. Others are formed in local tissue areas and cause only local circulatory effects. Among the most important of the humoral factors that affect circulatory function are those described in the following sections.

VASOCONSTRICTOR AGENTS

 Norepinephrine and Epinephrine. Norepinephrine is an especially powerful vasoconstrictor hormone; epinephrine is less so and in some tissues even causes mild vasodilation. (A special example of vasodilation caused by epinephrine is that which occurs to dilate the coronary arteries during increased heart activity.)

When the sympathetic nervous system is stimulated in most parts of the body during stress or exercise, 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. These hormones then circulate to all areas of the body and cause almost the same effects on the circulation as direct sympathetic stimulation, thus providing a dual system of control: (1) direct nerve stimulation and (2) indirect effects of norepinephrine and/or epinephrine in the circulating blood.

Angiotensin II. Angiotensin II is another powerful vasoconstrictor substance. As little as one millionth of a gram can increase the arterial pressure of a human being 50 mm Hg or more.

The effect of angiotensin II is to powerfully constrict the small arterioles. If this constriction occurs in an isolated tissue area, the blood flow to that area can be severely depressed. However, the real importance of angiotensin II is that it normally acts on many of the arterioles of the body at the same time to increase the total peripheral resistance and to decrease sodium and water excretion by the kidneys, thereby increasing the arterial pressure. Thus, this hormone plays an integral role in the regulation of arterial pressure, as is discussed in detail in Chapter 19.

Vasopressin. Vasopressin, also called antidiuretic hormone, is even more powerful than angiotensin II as a vasoconstrictor, thus making it one of the body’s most potent vascular constrictor substances. It is formed in nerve cells in the hypothalamus of the brain (see Chapters 29 and 76) but is then transported downward by nerve axons to the posterior pituitary gland, where it is finally secreted into the blood.

It is clear that vasopressin could have enormous effects on circulatory function. Yet, because only minute amounts of vasopressin are secreted in most physio logical conditions, most physiologists have thought that vasopressin plays little role in vascular control. However, experiments have shown that the concentration of circulating blood vasopressin after severe hemorrhage can increase enough to raise the arterial pressure as much as 60 mm Hg. In many instances, this action can, by itself, bring the arterial pressure almost back up to normal.

Vasopressin has the major function of greatly increasing water reabsorption from the renal tubules back into the blood (discussed in Chapter 29) and therefore helps to control body fluid volume. That is why this hormone is also called antidiuretic hormone.

VASODILATOR AGENTS

Bradykinin. Several substances called kinins cause powerful vasodilation when formed in the blood and tissue fluids of some organs.

The kinins are small polypeptides that are split away by proteolytic enzymes from α2-globulins in the plasma or tissue fluids. A proteolytic enzyme of particular importance for this purpose is kallikrein, which is present in the blood and tissue fluids in an inactive form. This inactive kallikrein is activated by maceration of the blood, tissue inflammation, or other similar chemical or physical effects on the blood or tissues. As kallikrein becomes activated, it acts immediately on α2-globulin to release a kinin called kallidin that is then converted by tissue enzymes into bradykinin. Once formed, bradykinin persists for only a few minutes because it is inactivated by the enzyme carboxypeptidase or by converting enzyme, the same enzyme that also plays an essential role in activating angiotensin, as discussed in Chapter 19. The activated kallikrein enzyme is destroyed by a kallikrein inhibitor also present in the body fluids.

Bradykinin causes both powerful arteriolar dilation and increased capillary permeability. For instance, injection of 1 microgram of bradykinin into the brachial artery of a person increases blood flow through the arm as much as sixfold, and even smaller amounts injected locally into tissues can cause marked local edema resulting from increase in capillary pore size.

Kinins appear to play special roles in regulating blood f low and capillary leakage of fluids in inflamed tissues. It also is believed that bradykinin plays a normal role to help regulate blood flow in the skin, as well as in the salivary and gastrointestinal glands.

Histamine. Histamine is released in essentially every tissue of the body if the tissue becomes damaged or inflamed or is the subject of an allergic reaction. Most of the histamine is derived from mast cells in the damaged tissues and from basophils in the blood.

Histamine has a powerful vasodilator effect on the arterioles and, like bradykinin, has the ability to increase greatly capillary porosity, allowing leakage of both fluid and plasma protein into the tissues. In many pathological conditions, the intense arteriolar dilation and increased capillary porosity produced by histamine cause tremendous quantities of fluid to leak out of the circulation into the tissues, inducing edema. The local vasodilatory and edema producing effects of histamine are especially prominent during allergic reactions and are discussed in Chapter 35.

VASCULAR CONTROL BY IONS AND OTHER CHEMICAL FACTORS

Many different ions and other chemical factors can either dilate or constrict local blood vessels. The following list details some of their specific effects:

1. An increase in calcium ion concentration causes vasoconstriction because of the general effect of calcium to stimulate smooth muscle contraction, as discussed in Chapter 8.

 2. An increase in potassium ion concentration, within the physiological range, causes vasodilation. This effect results from the ability of potassium ions to inhibit smooth muscle contraction.

3. An increase in magnesium ion concentration causes powerful vasodilation because magnesium ions inhibit smooth muscle contraction.

4. An increase in hydrogen ion concentration (decrease in pH) causes dilation of the arterioles. Conversely, a slight decrease in hydrogen ion concentration causes arteriolar constriction.

 5. Anions that have significant effects on blood vessels are acetate and citrate, both of which cause mild degrees of vasodilation.

6. An increase in carbon dioxide concentration causes moderate vasodilation in most tissues but marked vasodilation in the brain. Also, carbon dioxide in the blood, acting on the brain vasomotor center, has an extremely powerful indirect effect, transmitted through the sympathetic nervous vasoconstrictor system, to cause widespread vasoconstriction throughout the body.

Most Vasodilators or Vasoconstrictors Have Little Effect on Long-Term Blood Flow Unless They Alter the Metabolic Rate of the Tissues. In most cases, tissue blood flow and cardiac output (the sum of flow to all of the body’s tissues) are not substantially altered, except for a day or two, in experimental studies when one chronically infuses large amounts of powerful vasoconstrictors such as angiotensin II or vasodilators such as bradykinin. Why is blood flow not significantly altered in most tissues even in the presence of very large amounts of these vasoactive agents?

To answer this question we must return to one of the fundamental principles of circulatory function that we previously discussed—the ability of each tissue to auto regulate its own blood flow according to the metabolic needs and other functions of the tissue. Administration of a powerful vasoconstrictor, such as angiotensin II, may cause transient decreases in tissue blood flow and cardiac output but usually has little long-term effect if it does not alter metabolic rate of the tissues. Likewise, most vasodilators cause only short-term changes in tissue blood flow and cardiac output if they do not alter tissue metabolism. Therefore, blood flow is generally regulated according to the specific needs of the tissues as long as the arterial pressure is adequate to perfuse the tissues.

اخر الاخبار

اخبار العتبة العباسية المقدسة

شعبة الحرم الشريف تستعد لاستقبال زائري النصف من شهر شعبان

العتبة العباسية المقدسة تنشر لافتات الفرح بمناسبة ذكرى ولادة الإمام المهدي (عجّل الله فرجه)

العتبة العباسية المقدسة تفتتح التسجيل لتأدية الزيارة بالنيابة في ليلة النصف من شعبان

قسم المقام يعلن جاهزيّته لاستقبال زائري النصف من شعبان

المزيد

الآخبار الصحية

الصحة العالمية تكشف حقيقة انتشار فيروس نيباه خارج الهند

متى يصبح محيط الخصر "مؤشر خطر"؟

دراسة تكشف دور "العوامل الوراثية" في تحديد عمر الإنسان

رائحة كريهة في الجسم.. "علامة خفية" أخطر مما تتصور

المزيد

الآخبار التكنلوجية

مايكروسوفت تكشف عن الجيل الثاني من شرائحها للذكاء الاصطناعي

خرافة "ثمانية أكواب يوميا".. كم من الماء يحتاج جسمك فعليا؟

هل توجد حياة خارج كوكبنا؟.. اكتشاف جديد يثير اهتمام العلماء

اكتشاف الخلايا المسؤولة عن فقدان ذاكرة الطفولة

المزيد

مواضيع ذات صلة

Summary of Causes of Extracellular Edema

Determination of Volumes of Specific Body Fluid Compartments

Constituents of Extracellular and Intracellular Fluids

Pathophysiology of Hydroelectrolytic Disorders

Volume and Osmolality of Extracellular and Intracellular Fluids in Abnormal States

Regulation Of Fluid Exchange And Osmotic Equilibrium Between Intracellular And Extracellular Fluid

BODY FLUID COMPARTMENTS

الأمراض الناتجة عن خلل في الجهاز المناعي

أنواع الحساسية

الحساسية Allergy

وظيفة الجسم المضاد

خصوصية الأجسام المضادة Affinity