(see Baroreceptors)
1. High pressure baroreceptors
* Send signal to vasomotor centre via sensory neural pathway
2. Cardiopulmonary baroreceptors
Sympathetic nerve system innervation of vessels
--> Vasoconstriction and venoconstriction
NB:
BP changes in carotid and aortic artery
--> Signal input to vasomotor centre
--> Renal sympathetic nerve stimulation
--> beta1-adrenergic receptors on JG cells activated
--> cAMP increased (in JG cells)
--> Protein kinase A activated
--> Release of renin (from JG cells)
NB:
Alpha1-adrenergic receptors on JG cells are also stimulated
--> Afferent arteriole constriction
--> Decreased GFR and RBF
* However, most of this reduction is blunted by tubuloglomerular feedback
BP changes in renal afferent arterioles
--> Changes in JG cell deformation
--> Release renin (from JG cells)
NB:
Monitor the amount of NaCl in the filtrate entering DCT
Which depends on:
When amount of NaCl in the filtrate increases
--> Osmotic swelling of macula densa cells
--> Release of transmitter agent locally
* [WG21:p462] Possibly nitric oxide (NO)
--> Renin production from JG cells decrease
NB:
Renin release from JG cells
--> Renin converts angiotensinogen to angiotensin I
--> Angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II
--> Angiotensin II causes vasoconstriction
--> Reinforce vasoconstriction by sympathetic stimulation
* Slower onset (minutes)
Angiotensin II acts directly on JG cells to inhibit renin release
NB:
Kidney determines ECF volume (by controlling sodium and water)
--> Blood volume
--> Blood pressure
Thus, vasomotor centre is not involved in long term control