Blood Pressure Regulation Flashcards
Maintaining blood pressure: Short-term regulation
Neural controls: alter CO and R (resistance) to adjust for short-term BP fluctuations
Location: nervous system
- Baroreceptors: pressure receptors
These report to the medula oblengota when:
a. When hypertensive, baroreceptors are: stimulated or triggered
b. Cardiac center responds by: performing cardioinhibition (when we need to raise our BP -> Stimulated)
c. Vasomotor center responds by: inhibited to allow vasodilation. Resistance goes down and BP goes down.
d. Results: lowers HR, low R = lower BP = back to normal
e. Opposite events take place when hypotensive.
- Chemoreceptors: chemical receptors located close to baroreceptors.
a. Chemoreceptors detect the following:
i. Hypercapina (elevated CO2)
ii. Acidosis (low pH)
iii. Hypoxia
- Chemoreceptors: chemical receptors located close to baroreceptors.
b. Under these chemical conditions, the chemoreceptors will: activate cardiac center to perform cardioacceleration, trigger vasomotor center for vasoconstriction which makes R go up thus increasing our HR.
- Chemoreceptors: chemical receptors located close to baroreceptors.
c. Chemoreceptors stimulate an increase in BP to push more blood to the pulmonary circuit. To allow the gas exchange to go into lungs.
- Chemoreceptors: chemical receptors located close to baroreceptors.
d. Doing so helps flush the CO2 out of the bloodstream and bring more O2 into the bloodstream.
- Cerebrum and hypothalamus: higher brain centers can also alter BP
a. Cerebrum: mood, thoughts, emotions. These are your conscious controls which make your BP go up.
b. Hypothalamus: mediate stress testing through the fight or flight (ANS) mechanism when the body is active or in motion. These are your unconscious controls and involuntary in nature.
ii. Hormonal controls: hormonal cues can also alter BP in order to adjust to moment to moment fluctuations
- Hormones that elevated BP:
a. Epinephrine and norepinephrine: your adrenaline rush. Vasoconstrictors raise R and raise HR contractility
b. Angiotensin II: Powerful Vasoconstrictor which raises R which raises BP. triggers the release of ADH and aldosterone.
c. anti-diuretic hormone (ADH): vasorestrictor = increased R = increased BP. Affects kidneys and causes water retention
d. In summary: HIGH HR, SV, CO, R (VASOCONSTRICTION), V (VOLUME) = HIGH BP
ii. Hormonal controls: hormonal cues can also alter BP in order to adjust to moment to moment fluctuations
- Hormone that decreases BP:
a. Atrial natriuretic peptide (ANP): Makes R go down, which makes BP go down.
* antagonist to aldosterone
Antagonist= to block; prevents your BP from going up.
b. Maintaining blood pressure: long-term renal regulation (kidneys do the work)
i. Direct renal regulation
- When BP is low, the kidneys will: decrease filtration rate
- When less urine is excreted, fluid is retained in the body
- Fluid retention = increased volume = increased pressure
ii. [SUPER IMPORTANT]
Indirect renal regulation: RAAS
- RAAS stands for: renin-angiotensin aldosterone system
- When BP is low, the kidneys release an enzyme called RENIN (biological catalyst)
- Renin initiates the conversion of the liver hormone called ANGIOTENSINOGEN into ANGIOTENSIN I
- ANGIOTENSIN I is converted into ANGIOTENSIN II by ACE (angiotensin converting enzyme, from the lungs)
- (Effects of angiotensin II) angiotenson II is a multi-taskimg hormone. It’s activation will lead to:
a. Thirst reflex: increases fluid volume to increase BP
INCREASED VOLUME= INCREASED BP
b. Vasoconstriction: increases R to increase BP
c. Aldosterone releases from adrebal gland: increased slat retention by the kidneys to increase water retention to increase BP (THINK OSMOSIS)