It commonly causes hypertension due to increased renin secretion.

It has no significant impact on blood pressure regulation.

It results in episodic hypertension due to intermittent cortisol release.

It leads to hypotension due to cortisol and aldosterone deficiency.

it increases in response to mental stress

it decreases in response to painful stimuli

it increases in response to head-out water immersion

it decreases in patients with postural tachycardia syndrome in response to head-up tilt

decreased venous return and decreased stroke volume

increased venous return and increased stroke volume

increased venous return and decreased stroke volume

decreased venous return and increased stroke volume

An organ’s ability to maintain local blood flow in the face of changes in arterial pressure.

Arterioles constrict when they are exposed to lower levels of arterial pressure.

A mechanism that dominates local control of blood flow in the skin.

A theory about the development of hypertension that is opposed to Guyton’s ‘kidney – body fluid mechanism of long-term blood pressure control’.

acetylcholine

Renin

noradrenaline

gamma amino butyric acid (GABA)

aldosterone

angiotensin II induced vasoconstriction

capillary fluid shift

the kidney-body fluid mechanism

Cardiac baroreceptor firing decreases.

Water is absorbed through the skin.

Renal sympathetic nerve activity increases, leading to renin release.

 Atrial natriuretic peptide is released from the heart.

fear of causing low blood pressure in elderly patients and increasing the risk of falls and fractures

combination therapy, appropriately taken, is ineffective

drug induced side effects

lack of regular blood pressure monitoring

acetylcholine

gamma aminobutyric acid

excitatory amino acids

asparate

When the pressure difference between each end of the blood vessel is doubled

Doubling the length of vessel

Doubling blood viscosity

Halving the radius of the vessel