Hormonal changes

Vasopressin secretion

An important increase in plasma arginine vasopressin concentrations during ventilation with PEEP has been described in both animal and human studies. Vasopressin release probably occurs as a consequence of deactivation of atrial and aortic baroreceptors by the increase in intrathoracic pressure and decrease in aortic pressure. However, the quantitative role of vasopressin in PEEP-induced antidiuresis has yet to be clearly evaluated. Extremely high levels of vasopressin were observed when no volume restoration was undertaken during ventilation with PEEP, while normal levels were found with concurrent volume expansion. This could be due to the role of vasopressin as a systemic vasoconstrictor involved in circulatory homeostasis, rather than to its direct effects on renal proximal tubules.

Renin-angiotensin-aldosterone system

Plasma renin activity is elevated during ventilation with PEEP. Decreases in renal perfusion pressure and stimulation of sympathetic activity stimulate the release of renin from the kidney. Renin stimulates the production of angiotensin I from its substrate angiotensinogen by the action of angiotensin-converting enzyme. Angiotensin II increases the mean arterial blood pressure and systemic vascular resistance and decreases the glomerular filtration rate by constricting afferent glomerular vessels and mesangial cells. In addition, angiotensin II is a direct stimulator of tubular renal sodium reabsorption. It also stimulates the adrenal cortex to release aldosterone, which causes water retention and increased sodium absorbtion in the distal tubule of the nephrons.

Atrial natriuretic factor

Atrial natriuretic factor is a peptide hormone that is synthethized, stored, and secreted by the cardiac atria. It acts on the kidney to increase urine flow and sodium excretion, and may also enhance the glomerular filtration rate. Atrial natriuretic factor also antagonizes both the release and endorgan effects of vasopressin, renin, and aldosterone. Atrial distension is a major mechanism of atrial natriuretic factor secretion and, conversely, atrial compression can diminish the production of this hormone. Decreased atrial natriuretic factor secretion during ventilation with PEEP has been described in several human and animal studies. However, the absence of any modification in atrial natriuretic factor secretion during ventilation with 15 cmH 2O PEEP has recently been reported. These conflicting results may be due to differences in atrial transmural pressures and sampling sites (arterial versus atrial).

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