bp regulation & htn Flashcards
Difference in bp between a patients right and left arm is a sign of
vascular disease!
Why is hypertension bad?
It damages blood vessels throughout the entire body, affecting multiple systems.
Ex) Heart, brain, renal failure, retinopathy, peripheral vascular disease
Mechanisms of hypertension
-
Chronic positive salt & water balance
- Excessive salt; diseased kidney; messed up hormones; etc
- Overactive nervous system sending signals to heart, kidney, and blood vessels to retain salt
-
Incorrect responses of hormones that normally regulate salt and water balance & cardiovascular system
- Increased heart contractility; vasoconstriction; decreased blood flow to kidney reducing salt excretion
Most monogenetic causes of hypertension involves
Inappropriate Na+ reabsorption by the kidneys
Ex) Aldosteronism, liddle’s syndrome (excess Na+ channel activity), etc
Hypertension & Kidney disease can cause each other.
How does eating excessively salty food cause hypertension?
Eating too much salt can decrease your kidney’s Na+ excretory capability –> increased ECFV & BV
–> chronic increases in ECFV & BV or decreases in vascular capacitance will cause hypertension
How does increased [NaCl] lead to concentrated urine and thirst?
ADH gets released –> thirst & concentrated urine
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Whereas, if [NaCl] drops, then ADH gets inhibited.
Osmolality is rapidly regulated by adjusting
the ECFV by peeing
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Salt-resistant patients
When they increase their salt intake, they do have increased cardiac output since their ECFV increases (like normal).
However, they have decreased vascular resistance to accommodate for this increased cardiac output –> won’t develop hypertension
The most important regulatory mechanism of Na+ excretion is
GFR
- Autoregulatory mechanisms: higher bp, the greater afferent arteriole resistance to maintain RBF and GFR.
- NO from vascular smooth muscle cells maintains RBF and normal salt excretion
What stimulates reabsorption at the proximal tubule?
Ang II
Adrenergic agents
Increased luminal flow or solute delivery
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What stimulates reabsorption at the thick ascending limb?
ADH
Adrenergic agents
Mineralcorticoids
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What diuretics work at the distal tubule and connecting tubule cells?
Thiazides block the Na/Cl cotransporter
Amiloride blocks the apical Na+ channels, and at higher concentrations, the Na/H exchanger
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What stimulates reabsorption at the collecting duct?
Aldosterone
Antidiuretic hormone
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Pressure natriuresis
The higher your blood pressure, the higher Na+ excretion.
However, whether your salt status (deplete or replete) determines how much Na you’ll excrete at any given pressure.
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The impact of nitric oxide on pressure natriuresis
It promotes sodium excretion when bp is high
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COX1 & 2 are constitutively expressed in the kidney.
What upregulates COX2?
- Volume restriction
- High renin states ( need to compensate)
- Salt restriction
- ACE inhibition
- diuretic therapy
- renovascular htn
Giving an NSAID would have what effect on GFR and renal plasma flow?
Decreases both GFR & RBF because you don’t have prostaglandins to vasodilate. Thus, the RAS system is unopposed and going to vasoconstrict, decreasing both.
ANP
- Vasodilates
- Decreases aldosterone, renin, and Na reabsorption
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Beta blockers & calcium blockers
reduce blood vessel constriction
(remember that the sympathetic mechanism relies on norepi workign on a B receptor)