Create and Maintain high interstitial osmolality in the medulla.
Made up of 3 components:
1. Active Countercurrent Multplication: Outer medulla
2. Passive Countercurrent multiplication: Urea recycling, takes place in inner medulla
3.Countercurrent exchange
In vasa rectae, prevents dissipation of medullary interstitial gradient.
Active
Passive
Countercurrent
Renal Concentrating Ability
Nota:
Factors include
Length of the loop of Henle,
% of Long loops
Availabiluty of urea
Rate of flow in LH
Rate of flow in collecting duct
Blood flow in vasa recta
Loop diuretics
Diseases which would affect any of the structures in medulla
Antidiuretic Hormone
Nota:
Known as ADH, arginine vasopressin (AVP)
Its an octapeptide. produced ny nerve cells in the supraoptic a nd the paraventricular nuclei of the hypothalamus and near area of thirst.
Osmoreceptors
Nota:
Located int he lamina terminals near hypothalamus.
Stimulated by plasma osmolality. A small elevation will result in a ADH release in several folds.
A fall will result in cellular swelling and inhibition of ADH release.
Haemoreceptors
Nota:
Fall in blood volume/pressure stimulates release, detected by low pressure or high pressure baroreceptors.
Release
Nota:
Triggers could be cold, surgery anaestesia, haemorrhage, pain, emo, nausea, vomit.
Inhibition could be
ANP (atrial neutropeptide)
Aquaporins
Nota:
Comes in two forms.
Orthodox: Only let water in.
AQP1,2,4,5,6,8 ( AQP1,2,4 are more important)
Cocktails: Also known as aqua glycerol porins, they let water but also urea and other proteins and other stuff.
AQP3,7,9,10
Cell Reaction during Hypertonicity
Sodium balance
Nota:
Intake is thru diet.
Output in sweat, faeces, urine.
Urine output is regulated according to need
Detection
Nota:
Detected via changes in extracellular volume.
Increase in Na intake will lead to subsequent increase plasma osmolality, increase in thirst and water intake. Increase in ADH release and increase water retention
ECV
Nota:
Na intake is sense via effective circulating volume rather than ECFV.
Related to the volume and the pressures in CVS, depends on cardiac output.
Changes are detected via:
Low pressure volume receptors: in the pulmonary vasculature, atria, great veins.
High pressure baroreceptors in the carotid sinus, aortic arch, the juxtaglomerular apparatus.
Hence the afferent mechanisms, will affect the hypothalamus, and change the efferent mechanisms i.e change sympathetic nerve activity, and change various hormones.