HYPERTENSION 2

• 120/80
• 130/89
• 140/90 (one med)
• 160/100 (one or two meds)
• 180/110 or greater

SBP

Marked or shapr increase in  DBP to 120mm Hg

• No end organ damage evident
• Can reduce BP over hours to days

• End organ damage
• BP needs decrease within several min to hours

Aortic arch and carotid sinus

Smooth muscle cells within walls of arterioles in  skin, mucosa, viscera, kidneys and within walls of veins- causes vasoconstriction to increase BP.

Cells of SA node and AV node.  Increase HR, conductivity, force of contraction and increase CO which increases BP.

• 1.  Decrease in NaCl transport in the ascending limb  of the loop of Henle.
• 2.  Decrease pressure or stretch within the renal afferent arteriole (baroreceptor mechanism).
• 3.  Sympathetic NSstimulation of renin secreting cells via  B1 adrenoreceptors.

RENIN SECRETION IS INHIBITED BY THE OPPOSITE OF THE THE ABOVE FACTORS.

• 1.  Low BP detected by juxtaglomuerular cells in renal afferent arterioles.
• 2.  Renin release by renal affernt arterioles.
• 3.  Renin stimulates production of Angiotensin I.
• 4.  Angiotensin I turns into Angiotensin II
• 5.  ATI (brain, renal, nyocardial, vascular, and adrenal tissue) and ATII (brain, adrenal medulla, and uterine tissue) receptors stimulated.
• 6.  Sympathetic stimulation of cardia system- direct vasoconstriction, increase epinephrine release from adrenal medulla, and increase in sympathetic activity.
• 7.  Increased release of aldosterone which stimulates Na and K pumps in renal tubules.

• *HCTZ and metolazone
• *MOA- decreases plasma volume
• *Lowers BP 10-15 mm Hg in most pts
• *Sometimes used with vasoldilator or sympathomimetic drugs.
• *Decrease potassium, increase uric acid, increase glucose, increase lipid levels, decrease magnesium levels.

• *Decreases potassium, increase uric acid, increase glucose, increase lipid levels, decreace mag levels
• * 1-2 times more potent than HCTZ for BP