The Raas

The renin-angiotensin-aldosterone system contributes to the regulation of arterial

pressure primarily via the vasoconstrictor properties of angiotensin II and the sodium-
retaining properties of aldosterone. Renin is synthesized as an enzymatically inactive
precursor, prorenin in the Renal system. There are three primary stimuli for renin
secretion:

(1) decreased NaCl transport 

(2) decreased pressure in the kidney
(3) Sympathetic nervous system stimulation of renin-secreting cells via
β1 adrenoreceptors

Renin secretion is inhibited by increased NaCl transport, by increased stretch within

the renal afferent arteriole, and by β 1 receptor blockade. In addition, angiotensin II
directly inhibits renin secretion Once released into the circulation, active renin cleaves
a substrate, angiotensinogen, to form angiotensin I, A converting enzyme, located
primarily but not exclusively in the pulmonary circulation, converts angiotensin I to
the active octapeptide, angiotensin II

AUTONOMIC NERVOUS SYSTEM

Adrenergic reflexes modulate blood pressure over the short term, and adrenergic
function, in concert with hormonal and volume-related factors, contributes to the
long-term regulation of arterial pressure. Norepinephrine, epinephrine, and dopamine
all play important roles in tonic and phasic cardiovascular regulation.
adrenergic receptors have been divided into two principal types: α and β. These types
have been differentiated further into α 1, α2, β1, and β2 receptors.

Some receptors we have in some organs, for example The kidney, the blood vessel
and the hearth they send signals (Low blood pressure, lack of oxygen or blood) to the
Brain stem or the medulla oblongata, from there it goes to our brain and it sends some
electric signals in response, those signals goes to the kidney, the hearth and the
adrenal gland. It makes the kidney to retain water and sodium, the hearth beats faster
and the adrenal gland release catecholamine that enhances the mentioned effects

Endothelin
ET-1 is synthesized in human endothelial cells by a dual secretory pathway. ET-1 is continuously released
from the small vesicles of the constitutive pathway to interact with ET receptors to contribute to
vasomotor tone. ET-1 is also released from the regulated pathway in response to external stimuli from
Weibel-Palade bodies that are unique to endothelial cells.