control of blood vessels: peripheral resistance

Question 1

general: peripheral resistance

Answer 1

all resistance vessels innervated by SNS. when arterial pressure falls, SNS nerve terminals release noradrenaline onto the VSMCs, causing them to contract.
Contraction is mediated by α1-adrenergic receptors acting via the IP3 signalling pathway, causing Ca2+ release from the sarcoplasmic reticulum .

Question 2

contraction mediation

Answer 2

Contraction is mediated by α1-adrenergic receptors acting via the IP3 signaling pathway, causing Ca2+ release from the sarcoplasmic reticulum .

Question 3

resistance relations

Answer 3

• directly related to length of the vessel
• directly related to viscosity of the fluid
• inversely related to vessel radius- this is the most important factor.

Arterioles are the ‘resistance vessels’

Question 4

what does blood vessel radius depend on

Answer 4

1) active tension exerted by smooth muscle (vascular smooth muscle)- many factors modulate
2) passive elastic elastic properties of wall (elastin and collagen)
3) blood pressure inside vessel and pressure outside the vessel

Question 5

laPlace’s law

Answer 5

• distending pressure - wall tension / radius
• wall tension = radius x pressure
• this is why larger blood vessels tend to rupture
• distending pressure = intra - extravascular pressure

Question 6

factors affecting vascular smooth muscle contraction

Answer 6

noradrenaline:

• alpha2 and aplha1- vasoconstriction
• beta2- vasodilation

Question 7

hormonal control

Answer 7

• ANP and BNP (direct vasodilation affect and reduction in renin)
• Ang II (Ang-II binds to angiotensin AT1 receptors on VSMCs, which couple to the IP3 signalling pathway.)
• ADH (mechanism ADH binds to vasopressin V1a receptors on VSMCs, ADH binds to vasopressin V1a receptors on vascular smooth muscle cell –(VSMCs)
• Adrenaline Binds to α1-adrenergic receptors on VSMCs to potentiate the direct SNS-mediated vasoconstriction.

Question 8

adrenal cortex and adrenaline

Answer 8

Zona glomerulosa – mineralocorticoids, eg, aldosterone
Zona fasciculata - glucocortocoids, eg, cortisol
Zona reticularis - gonadocorticoids, eg, oestrogens

Medulla – adrenaline, noradrenaline (chromaffin cells)

Question 9

mineralocorticoids

Answer 9

secreted by the outermost region of the adrenal cortex. The principal mineralocorticoid is aldosterone, which acts to conserve sodium ions and water in the body.

Question 10

glucocorticoids

Answer 10

secreted by the middle region of the adrenal cortex. The principal glucocorticoid is cortisol, which increases blood glucose levels.

Question 11

gonadocortacoids

Answer 11

secreted by the innermost region.
Androgens and oestrogens are secreted in minimal amounts in both sexes by the adrenal cortex, but their effect is usually masked by the hormones from the testes and ovaries. In females, the masculinization effect of androgen secretion may become evident after menopause, when oestrogen levels from the ovaries decrease.
All these cortical hormones are produced from a common precursor – cholesterol.

Question 12

describe how factors released from the endothelium can modulate vascular tone.

Answer 12

The endothelial lining of resistance vessels acts as an intermediary for a number of vasoactive compounds, including nitric oxide (NO), prostaglandins (PGs), endothelium-derived hyperpolarizing factor (EDHF), and endothelins.

Question 13

prostaglandins

Answer 13

• formed via cyclooxygenase

The endothelium is an important source of a number of vasoactive PGs, which it synthesizes from arachidonic acid.

Dilators: PGE (PGE1, PGE2, and PGE3) and PGI2 (prostacyclin) relax VSMCs in many vascular beds,

Constrictors: whereas PGF (PGF1, PGF2α, PGF3α) and thromboxane A2 are vasoconstrictors.

PGI2: Works in opposition to TXA2 .

Question 14

features of chemical mediators

Answer 14

Vasodilation: histamine, nitric oxide, PGI2
Vasoconstriction: thromboxane A2(TXA2)
Increasing venular permeability: histamine, bradykinin, LTC4, LTD4, LTE4, C3a, and C5a
Producing Pain: PGE2, bradykinin
Producing fever: PGE2, IL-1, TNF
Chemotaxis: C5a, LTB4, IL-8.

Question 15

nitric oxide

Answer 15

• a potent vasodilator, acts on both arteries and veins
• also known as endothelium-derived relaxing factor EDRF, synthesised by a constitutive endothelial NO synthase, following rise in intracellular Ca2+ concentrations
• NO half life is 10 seconds- actions remain highly localised

Question 16

nitroglycerin and related nitrates

Answer 16

commonly used to relieve the pain of angina. nitrates break down to release NO in vivo, causing arterial and venous vasodilation to lower ventricular preload and afterload. reducing cardiac workload restores the balance between O2 demand and supply relieves the angina.

Question 17

metabolic factors

Answer 17

cells continuously release various metabolic by-products, including adenosine, lactate, K+, H+, and co2.
some metabolites act directly on VSMCs, whereas others act through endothelial cells, but all cause the VSMCs to relax and the vessels to dilate. blood flow increases as a result, simultaneously providing the tissues with the nutrients they need and also carrying away metabolites.

Question 18

myogenic mechanisms

Answer 18

• resistance vessels inn many circulations constrict reflexively when intraluminal pressures rise.
  contraction is mediated by stretch-activated Ca2+ channels in the VSMC membranes and may protect capillaries from surges in arterial pressures.