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Auto Regulation

The ability of an organ to regulate its blood flow (on its own independent of nervous ystemic influences ) with changes in perfusion pressure (with in a range)Many organs show auto regulation.

Example : Brain, Kidney, Skeletal muscle, liver, heart , etc.


Skin does not show autoregulation.

Theories of auto regulation


1. Myogenic:- This depends upon the inherent property of the smooth muscle to contract ,when stretched. More the perfusion pressure, the more it contracts to decrease the calibre of the vessel and hence to decrease the blood flow.


2. Metabolic:- Less the perfusion pressure, more is the accumulation of local metabolites which can dilate the vessel and thus increase blood flow.


3. Tissue pressure theory – This is applicable in encapsulated organs e.g. kidney Some of the vasodilator metabolites are O2, CO2, pH, Osmolality, temperature, K+ , Adenosine, Lactate etc.


Note:- The local effect of hypoxia & hypercapnia is vasodilatation in all the blood vessels except pulmonary vessels where they cause vasoconstriction.

Circulating hormones

These can be vasoconstrictors / vasodilators.

                                                                      Circulating hormones



Epinephrine (except in skeletal muscle and liver)

Norepinephrine, AVP , Angiotensin II

Neuropeptide Y

Epinephrine in skeletal muscle and liver

CGRPϒ Substance P, Histamine, ANP, VIP


Examples of vasoconstrictors

  1. Pinephrine /Norepinephrine
  2. Norepinephirine causes generalized vasoconstriction where as epinephrine dilates the vessels in skeletal muscle and liver.




Systolic B.P

Diastolic B.P.

Mean arterial Pressure

Only slight

Pulse pressure

only slight


Heart rate

Reflex bradycardia

Cardiac output

  1. Dopamine: Causes vasoconstriction everywhere except in renal vessels where it causes renal vasodilatation.
  2. Angiotensin II: It causes generalized vasoconstriction , increases water intake and stimulates aldosterone secretion.

Kinin system   

  1. The kinin system generates vasoactive peptides from plasma proteins, called kininogens, by the action of specific proteases called kallikreins. Activation of the kinin system results in the release of the vasoactive nonapeptide bradykinin.
  2. Bradykinin increases vascular permeability and causes contraction of smooth muscle, dilation of blood vessels, and pain when injected into the skin. These effects are similar to those of histamine.
  3. It is triggered by the activation of Hageman factor (factor XII of the intrinsic clotting pathway) upon contact with negatively charged surfaces, such as collagen and basement membranes.
  4. A fragment of factor XII (prekallikrein activator, or factor XIIa)is produced, and this converts plasma prekallikrein into an active proteolytic form, the enzyme kallikrein. The latter cleaves a plasma glycoprotein precursor, high-molecular-weight kininogen, to produce bradykinin.
  5. Bradykinin is degraded by:

  1. Kininase I-a carboxy peptidase that removes carboxy terminal Arg
  2. Kininase II-removes Phe-Arg from carboxy terminal Kininase II is
  3. ympathetic vasodilator system
  1. Site: Vessels of skeletal muscles
  2. Pathway: From the cortex to the vessels .It does not influence the vasomotor center in the medulla.
  3. Neurotransmitter: The neuro transmitter at their postganglionic neurons is acetylcholine.
  4. Functional role: It plays no role in the vasodilation in skeletal muscles during exercise;it may play a role in the vasodilation by the thought of exercise.

Triple Response: Red reaction, Wheal & Flare

1. When the skin is stroked more firmly with a pointed instrument, instead of the white reaction there is reddening at the site that appears in about 10 seconds (red reaction).It is due to release of Histamine. The initial redness is due to capillary dilation.

2. The, swelling (wheal) is local edema due to increased permeability of the capillaries and postcapillary venules, with consequent extravasation of fluid. It is again due to release of Histamine, bradykinin etc.


3. The redness spreading out from the injury (flare)is due to arteriolar dilation. Mediated via AXON REFLEX.


Axon Reflex-Peculiarities/Features

  1. It is a local reflex ; the impulse does not reach the spinal cord
  2. Antidromic conduction
  3. The neurotransmitter is substance P
  4. Produces vasodilatation and increased capillary permeability
  5. It is responsible for the ‘flare’ of triple reaction
  6. Asynaptic It is present even after total sympathectomy. The flare is absent in locally anesthetized skin and in denervated skin after the sensory nerves have degenerated.


Neural Regulation

The main cardiocascular ‘centre’ is in the medulla.There are 2 ‘centers’ viz

  1. Vasomotor centre (VMC)
  2. Cardio inhibitory centre (CIC)
  3. The VMC is in the rostral ventrolateral medulla (RULM); it has connection with the (inter mediolateral grey horn) of the spinal cord from which sympathetic innervation arises for the heart and blood vessels.
  4. The CIC is in fact the nucleus of the vagus . It innervates the heart. The nucleus ambiguus by the vagus is the CIC.

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