this Something', was Christened by them as renin' (a name which has been retained even almost 100 years after).

diseases of the kidney are related with edema and hypertension In 1898 Tiegersted and Bergam showed that saline exacts of kidney contans something which can riase BP, and this Something', was Christened by them as renin' (a name which has been retained even almost 100 years after). The turning point was in I934, when Harry Goldblatt ana his colleagues showed that partial occlusion of renal Artery (by ligation) in dogs produce hypertension Since this lead, tremendous amount of risearch with works have followed and at the time of wirting the. the consensus of opinion. in this area of physiology is as follows It is possible that a minimal state of activity of the renin anglotersin axis existe even ordenarly But under special circumstances ' (see below), renin is secreted in large Quantities and produces a chain of events as follows renin is produced from Juxta glomerular apparatus, JGA (recall. JGA = JG cells of Via walls of the afferent artenriole of the glomerulus - mesangial cells - macula densa. particularly from the JG cells the renin now acts on angiotensrogen, an 02 globulin present normaly in the plasma Previously, angiotensinogen was also known as hypertensinogen, particularly in the Latin American countries. angiotensinogen is now converted ed Into ingiotensin I angiotensin I is further converted into angiotensin II by converting enzyme, popularty abbreviated as ACE (angiotensin converting enzyme) by the clinicians and pharoacologisist. The lungs are rich in ACE and when angiostensin I rich blood flows through tne lungs, angiotensin II is thus formed Angiotensin II has many actions but most well known of them are its actions on (i) blood vessels and(ii)Na+,k+ and water regulation In recent times, the effects of angiotensin on(iii)myocardial contractily and (iv) on brain are receving great attention angiotensin II is further degraded into angiotensin IIl. which has a much weaker angiotensin like action The flow chart given below. summarises the above mentioned facts. What condition stimulate the renin secretion ? Answer follows i) Low perfusion pressure of blood in the kidneys Actually. by ligating the renal artery, Golabatt merely produced low BP in the afferent arterioles of the glomerulus Clinically renal arterial stenosis is associated with excessive activity of rerin angiotensin system and hypertension and the mechanism is same Further details are as follows :the JG cells, present in The waits of the afferent arterioles of the glomerulus, release renin. when the BP within These arterioles fall. The sensor (= which detects the fall of BP) is thus a baroreceptor. The means, when there is a generalised fall of BP (eg hemorrrhagic shock, severe diarrhea) there is excessive activity of the renin angiotansin system Indeed. in such patholagical states where BP is low and thus the brain is threatened by is chemia ang anoxia. this is a major compensatory mechanism i) A second method of stimulating renin secretion is, decreased delevery of na Into the region of macula densa of the distal tubule. For example, severe fall of systemic BP {say due to massive hemorrhage) will lead to fall of BP fall of glomerular BP fall of GFR fall of filtered load of na decreased delevery of Na in the region of macua densa renin secretion angiotensin) which leabs to arteriolar constriction Sodium retention (both causing restoration of BP) ( iii) Sympathetic stimulation also causes stimulation of renin secretion. The JG cells are supplied by sympathetic nerves (to be specific, adrenergic nerves) blockers thus reduce the renin angiotensin system activity effects of angiotensin 1. Angiotensin II is a powerful vasoconstrictor it causes a generalized vaso constriction,