63. Primary arterial hypertension.

Aethiology:

1. psycho-emotional tension;

2. inheritance;

3. salt excessive usage.

2 Pathogenetical conceptions:

1. dysregulatory – defects in arterial pressure regulative mechanisms;

2. membrane – hypertension is a result of primary changing in arterioles smooth myocytes.

Arterial hypertony stages according to dysregulatory concept:

1. hyperkinetic – minute cardiac volume increasing leads to arterial pressure rising up:

1. sympatho-adrenale system activation; results:

-heart minute volume increasing;

• total peripheral resistance increasing;

• renin releasing to blood after juxta-glomerular apparatus stimulation

2. renin-angiotensine system activation; results:

• arterioles smooth muscles contraction (angiospasm);

• CNS structures participating in arterial pressure regulating excitement;

• aldosterone releasing to blood with suprarenal gland glomerular zone cells;

1. aldosterone-vasopressine system activation; results:

• hyper-Na-emia;

• osmoreceptors activation;

• ADH secretion in hypothalamus;

• facultative water reabsorbtion enforcement in kidney;

• hypervolemy, heart minute volume increasing;

• hypertension;

3. hypokinetic – is characterized by arterioles irreversible changings as a result of which total 56eripheral resistance and arterial pressure are increased constantly; consequent stages:

   1. autoregulatory arterioles spasm – is a result of heart minute volume increasing; it is directed to blood stream constancy support in tissues (it prevents blood excessive amount appearance);

   2. arterioles smooth muscles hypertrophy (structural expression of smooth muscles hyperfunction at often spasms);

   3. arterioles spasm.

Membrane concept:

3. Ca-pumps defects in cellular membranes lead to Ca ions removal defects from cellular cytoplasm and their intracellular concentration increasing; it causes arterioles smooth muscles contracture (overcontraction) which leads to total peripheral resistance and arterial pressure rising up; besides, Ca-ions in cellular cytoplasm causes their injury and a predisposition to arteriolosclerosis development;

4. Na-K pumps activity inhibiting in smooth myocytes plasmatic membranes; particularly endogenous strophanthine-like factor can be found in patients (it inhibitis these pumps activity like heart glycosides); pumps disorders lead to Na content increasing in smooth myocytes and to their oedema which in turn result in: arterioles wall thickness and bed diminishing; smooth myocytes sensitivity increasing to endogenous catecholamines action; cells injury and following death with further arteriolosclerosis development.

64. Secondary arterial hypertension.

Aethiology:

1) kidney diseases (glomerulonephritis, pyelonephritis, polycystosis et al.);

2) suprarenal glands tumors (pheochromocytome, aldosterome);

3. heart and vessels injury (several heart vices, aortal coarctation or constriction);

4. nervous system diseases (bulbary poliomyelitis, encephalitis, brain concussion).

Mechanisms:

1) prolonged stress and psycho-emotional tension;

2) pressure of carotid and vertebral arteries;

3) renal artery or arteries constriction with tumor, scar;

4) renal artery occlusion with thromb, embol, tumor, atheroscleroic plaque;

5. hypovolemy at burning disease;

6) renal artery arms compression at inflammatory diseases;

4) kidney removal and transfer to haemodyalisis (renopryval hypertension) (depressor functions are switched off in kidney because of prostaglandines A and E, bradykinine, kallidine synthesis stoppage)

6. adrenaline injection;

7. hyperaldosteronism or Konn’s syndrome (cortex hyperplasy or tumor)

8. vasopressine injection;

9. suprarenal cortex removal;

10. mineralocorticoid therapy;

11. glucocorticoids lead to mineralocorticoids level increasing and thus to AP increasing (at Itsenko-Kushing’s syndrome);

12. hyperthyreosis – due to cardiac charge significant increasing;

13. disease of Itsenko-Kushing’s;

14. neuroses;

15. all pathological conditions delt with rheology disorders (particularly with hyperviscosity) because of loading increasing to heart and total peripheral resistance increasing.

3-6 – renovascular hypertension – renin-angiotensine-aldosterone mechanism.